Adapalene suppressed the proliferation of melanoma cells by S-phase arrest and subsequent apoptosis via induction of DNA damage
Malignant melanoma was the leading cause of mortality among the skin-associated cancer owing to its highly metastatic feature, increasing incidence and drug resistance requirement. Retinoids played important roles in the treatment of cancer via the activation of retinoid acid receptor (RAR) or retin...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Li, Hongyang [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2019transfer abstract |
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| Schlagwörter: |
Bexarotene (PubChem CID: 82146) Adapalene (PubChem CID: 60164) |
|---|
| Umfang: |
12 |
|---|
| Übergeordnetes Werk: |
Enthalten in: Mexican student-teachers’ “English” language praxicum: Decolonizing attempts - López-Gopar, Mario E. ELSEVIER, 2022, EJP, New York, NY [u.a.] |
|---|---|
| Übergeordnetes Werk: |
volume:851 ; year:2019 ; day:15 ; month:05 ; pages:174-185 ; extent:12 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.ejphar.2019.03.004 |
|---|
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ELV046301844 |
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| 520 | |a Malignant melanoma was the leading cause of mortality among the skin-associated cancer owing to its highly metastatic feature, increasing incidence and drug resistance requirement. Retinoids played important roles in the treatment of cancer via the activation of retinoid acid receptor (RAR) or retinoid X receptor (RXR). Our present study showed that the third-generation retinoid adapalene exhibited strong inhibitory effects on the proliferation of melanoma cells than other retinoids, such as all-trans-retinoic acid (ATRA), isotretinoin, acitretin and bexarotene, and adapalene exerted significant inhibitory effects on the colony formation of melanoma cells. Further study confirmed that adapalene treatment triggered dramatic S phase arrest and apoptosis, and S phase arrest was the potential mechanism of apoptosis induction. In addition, adapalene treatment dramatically regulated the expression of S phase-related protein, and increased the protein level of DNA damage marker，which were consistent with the results of the induction of the tail moment in comet assays. Meanwhile, DNA damage response was activated and the DNA repair pathway was simultaneously inhibited by adapalene treatment, which might furtherly potentiate S phase arrest and subsequent apoptosis. Taken together, these results showed that adapalene exhibited strong anti-cancer activity, and might be a candidate agent for the clinical treatment of melanoma. | ||
| 520 | |a Malignant melanoma was the leading cause of mortality among the skin-associated cancer owing to its highly metastatic feature, increasing incidence and drug resistance requirement. Retinoids played important roles in the treatment of cancer via the activation of retinoid acid receptor (RAR) or retinoid X receptor (RXR). Our present study showed that the third-generation retinoid adapalene exhibited strong inhibitory effects on the proliferation of melanoma cells than other retinoids, such as all-trans-retinoic acid (ATRA), isotretinoin, acitretin and bexarotene, and adapalene exerted significant inhibitory effects on the colony formation of melanoma cells. Further study confirmed that adapalene treatment triggered dramatic S phase arrest and apoptosis, and S phase arrest was the potential mechanism of apoptosis induction. In addition, adapalene treatment dramatically regulated the expression of S phase-related protein, and increased the protein level of DNA damage marker，which were consistent with the results of the induction of the tail moment in comet assays. Meanwhile, DNA damage response was activated and the DNA repair pathway was simultaneously inhibited by adapalene treatment, which might furtherly potentiate S phase arrest and subsequent apoptosis. Taken together, these results showed that adapalene exhibited strong anti-cancer activity, and might be a candidate agent for the clinical treatment of melanoma. | ||
| 650 | 7 | |a Bexarotene (PubChem CID: 82146) |2 Elsevier | |
| 650 | 7 | |a ATRA (PubChem CID: 444795) |2 Elsevier | |
| 650 | 7 | |a Adapalene (PubChem CID: 60164) |2 Elsevier | |
| 650 | 7 | |a Isotretinoin (PubChem CID: 5282379) |2 Elsevier | |
| 650 | 7 | |a Acitretin (PubChem CID: 5284513) |2 Elsevier | |
| 700 | 1 | |a Wang, Cheng |4 oth | |
| 700 | 1 | |a Li, Lingjun |4 oth | |
| 700 | 1 | |a Bu, Wenbo |4 oth | |
| 700 | 1 | |a Zhang, Mengli |4 oth | |
| 700 | 1 | |a Wei, Jun |4 oth | |
| 700 | 1 | |a Tao, Lei |4 oth | |
| 700 | 1 | |a Qian, Kun |4 oth | |
| 700 | 1 | |a Ma, Pengcheng |4 oth | |
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10.1016/j.ejphar.2019.03.004 doi GBV00000000000572.pica (DE-627)ELV046301844 (ELSEVIER)S0014-2999(19)30153-0 DE-627 ger DE-627 rakwb eng 370 VZ 5,3 ssgn Li, Hongyang verfasserin aut Adapalene suppressed the proliferation of melanoma cells by S-phase arrest and subsequent apoptosis via induction of DNA damage 2019transfer abstract 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Malignant melanoma was the leading cause of mortality among the skin-associated cancer owing to its highly metastatic feature, increasing incidence and drug resistance requirement. Retinoids played important roles in the treatment of cancer via the activation of retinoid acid receptor (RAR) or retinoid X receptor (RXR). Our present study showed that the third-generation retinoid adapalene exhibited strong inhibitory effects on the proliferation of melanoma cells than other retinoids, such as all-trans-retinoic acid (ATRA), isotretinoin, acitretin and bexarotene, and adapalene exerted significant inhibitory effects on the colony formation of melanoma cells. Further study confirmed that adapalene treatment triggered dramatic S phase arrest and apoptosis, and S phase arrest was the potential mechanism of apoptosis induction. In addition, adapalene treatment dramatically regulated the expression of S phase-related protein, and increased the protein level of DNA damage marker，which were consistent with the results of the induction of the tail moment in comet assays. Meanwhile, DNA damage response was activated and the DNA repair pathway was simultaneously inhibited by adapalene treatment, which might furtherly potentiate S phase arrest and subsequent apoptosis. Taken together, these results showed that adapalene exhibited strong anti-cancer activity, and might be a candidate agent for the clinical treatment of melanoma. Malignant melanoma was the leading cause of mortality among the skin-associated cancer owing to its highly metastatic feature, increasing incidence and drug resistance requirement. Retinoids played important roles in the treatment of cancer via the activation of retinoid acid receptor (RAR) or retinoid X receptor (RXR). Our present study showed that the third-generation retinoid adapalene exhibited strong inhibitory effects on the proliferation of melanoma cells than other retinoids, such as all-trans-retinoic acid (ATRA), isotretinoin, acitretin and bexarotene, and adapalene exerted significant inhibitory effects on the colony formation of melanoma cells. Further study confirmed that adapalene treatment triggered dramatic S phase arrest and apoptosis, and S phase arrest was the potential mechanism of apoptosis induction. In addition, adapalene treatment dramatically regulated the expression of S phase-related protein, and increased the protein level of DNA damage marker，which were consistent with the results of the induction of the tail moment in comet assays. Meanwhile, DNA damage response was activated and the DNA repair pathway was simultaneously inhibited by adapalene treatment, which might furtherly potentiate S phase arrest and subsequent apoptosis. Taken together, these results showed that adapalene exhibited strong anti-cancer activity, and might be a candidate agent for the clinical treatment of melanoma. Bexarotene (PubChem CID: 82146) Elsevier ATRA (PubChem CID: 444795) Elsevier Adapalene (PubChem CID: 60164) Elsevier Isotretinoin (PubChem CID: 5282379) Elsevier Acitretin (PubChem CID: 5284513) Elsevier Wang, Cheng oth Li, Lingjun oth Bu, Wenbo oth Zhang, Mengli oth Wei, Jun oth Tao, Lei oth Qian, Kun oth Ma, Pengcheng oth Enthalten in Elsevier López-Gopar, Mario E. ELSEVIER Mexican student-teachers’ “English” language praxicum: Decolonizing attempts 2022 EJP New York, NY [u.a.] (DE-627)ELV008405875 volume:851 year:2019 day:15 month:05 pages:174-185 extent:12 https://doi.org/10.1016/j.ejphar.2019.03.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 851 2019 15 0515 174-185 12 |
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10.1016/j.ejphar.2019.03.004 doi GBV00000000000572.pica (DE-627)ELV046301844 (ELSEVIER)S0014-2999(19)30153-0 DE-627 ger DE-627 rakwb eng 370 VZ 5,3 ssgn Li, Hongyang verfasserin aut Adapalene suppressed the proliferation of melanoma cells by S-phase arrest and subsequent apoptosis via induction of DNA damage 2019transfer abstract 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Malignant melanoma was the leading cause of mortality among the skin-associated cancer owing to its highly metastatic feature, increasing incidence and drug resistance requirement. Retinoids played important roles in the treatment of cancer via the activation of retinoid acid receptor (RAR) or retinoid X receptor (RXR). Our present study showed that the third-generation retinoid adapalene exhibited strong inhibitory effects on the proliferation of melanoma cells than other retinoids, such as all-trans-retinoic acid (ATRA), isotretinoin, acitretin and bexarotene, and adapalene exerted significant inhibitory effects on the colony formation of melanoma cells. Further study confirmed that adapalene treatment triggered dramatic S phase arrest and apoptosis, and S phase arrest was the potential mechanism of apoptosis induction. In addition, adapalene treatment dramatically regulated the expression of S phase-related protein, and increased the protein level of DNA damage marker，which were consistent with the results of the induction of the tail moment in comet assays. Meanwhile, DNA damage response was activated and the DNA repair pathway was simultaneously inhibited by adapalene treatment, which might furtherly potentiate S phase arrest and subsequent apoptosis. Taken together, these results showed that adapalene exhibited strong anti-cancer activity, and might be a candidate agent for the clinical treatment of melanoma. Malignant melanoma was the leading cause of mortality among the skin-associated cancer owing to its highly metastatic feature, increasing incidence and drug resistance requirement. Retinoids played important roles in the treatment of cancer via the activation of retinoid acid receptor (RAR) or retinoid X receptor (RXR). Our present study showed that the third-generation retinoid adapalene exhibited strong inhibitory effects on the proliferation of melanoma cells than other retinoids, such as all-trans-retinoic acid (ATRA), isotretinoin, acitretin and bexarotene, and adapalene exerted significant inhibitory effects on the colony formation of melanoma cells. Further study confirmed that adapalene treatment triggered dramatic S phase arrest and apoptosis, and S phase arrest was the potential mechanism of apoptosis induction. In addition, adapalene treatment dramatically regulated the expression of S phase-related protein, and increased the protein level of DNA damage marker，which were consistent with the results of the induction of the tail moment in comet assays. Meanwhile, DNA damage response was activated and the DNA repair pathway was simultaneously inhibited by adapalene treatment, which might furtherly potentiate S phase arrest and subsequent apoptosis. Taken together, these results showed that adapalene exhibited strong anti-cancer activity, and might be a candidate agent for the clinical treatment of melanoma. Bexarotene (PubChem CID: 82146) Elsevier ATRA (PubChem CID: 444795) Elsevier Adapalene (PubChem CID: 60164) Elsevier Isotretinoin (PubChem CID: 5282379) Elsevier Acitretin (PubChem CID: 5284513) Elsevier Wang, Cheng oth Li, Lingjun oth Bu, Wenbo oth Zhang, Mengli oth Wei, Jun oth Tao, Lei oth Qian, Kun oth Ma, Pengcheng oth Enthalten in Elsevier López-Gopar, Mario E. ELSEVIER Mexican student-teachers’ “English” language praxicum: Decolonizing attempts 2022 EJP New York, NY [u.a.] (DE-627)ELV008405875 volume:851 year:2019 day:15 month:05 pages:174-185 extent:12 https://doi.org/10.1016/j.ejphar.2019.03.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 851 2019 15 0515 174-185 12 |
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10.1016/j.ejphar.2019.03.004 doi GBV00000000000572.pica (DE-627)ELV046301844 (ELSEVIER)S0014-2999(19)30153-0 DE-627 ger DE-627 rakwb eng 370 VZ 5,3 ssgn Li, Hongyang verfasserin aut Adapalene suppressed the proliferation of melanoma cells by S-phase arrest and subsequent apoptosis via induction of DNA damage 2019transfer abstract 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Malignant melanoma was the leading cause of mortality among the skin-associated cancer owing to its highly metastatic feature, increasing incidence and drug resistance requirement. Retinoids played important roles in the treatment of cancer via the activation of retinoid acid receptor (RAR) or retinoid X receptor (RXR). Our present study showed that the third-generation retinoid adapalene exhibited strong inhibitory effects on the proliferation of melanoma cells than other retinoids, such as all-trans-retinoic acid (ATRA), isotretinoin, acitretin and bexarotene, and adapalene exerted significant inhibitory effects on the colony formation of melanoma cells. Further study confirmed that adapalene treatment triggered dramatic S phase arrest and apoptosis, and S phase arrest was the potential mechanism of apoptosis induction. In addition, adapalene treatment dramatically regulated the expression of S phase-related protein, and increased the protein level of DNA damage marker，which were consistent with the results of the induction of the tail moment in comet assays. Meanwhile, DNA damage response was activated and the DNA repair pathway was simultaneously inhibited by adapalene treatment, which might furtherly potentiate S phase arrest and subsequent apoptosis. Taken together, these results showed that adapalene exhibited strong anti-cancer activity, and might be a candidate agent for the clinical treatment of melanoma. Malignant melanoma was the leading cause of mortality among the skin-associated cancer owing to its highly metastatic feature, increasing incidence and drug resistance requirement. Retinoids played important roles in the treatment of cancer via the activation of retinoid acid receptor (RAR) or retinoid X receptor (RXR). Our present study showed that the third-generation retinoid adapalene exhibited strong inhibitory effects on the proliferation of melanoma cells than other retinoids, such as all-trans-retinoic acid (ATRA), isotretinoin, acitretin and bexarotene, and adapalene exerted significant inhibitory effects on the colony formation of melanoma cells. Further study confirmed that adapalene treatment triggered dramatic S phase arrest and apoptosis, and S phase arrest was the potential mechanism of apoptosis induction. In addition, adapalene treatment dramatically regulated the expression of S phase-related protein, and increased the protein level of DNA damage marker，which were consistent with the results of the induction of the tail moment in comet assays. Meanwhile, DNA damage response was activated and the DNA repair pathway was simultaneously inhibited by adapalene treatment, which might furtherly potentiate S phase arrest and subsequent apoptosis. Taken together, these results showed that adapalene exhibited strong anti-cancer activity, and might be a candidate agent for the clinical treatment of melanoma. Bexarotene (PubChem CID: 82146) Elsevier ATRA (PubChem CID: 444795) Elsevier Adapalene (PubChem CID: 60164) Elsevier Isotretinoin (PubChem CID: 5282379) Elsevier Acitretin (PubChem CID: 5284513) Elsevier Wang, Cheng oth Li, Lingjun oth Bu, Wenbo oth Zhang, Mengli oth Wei, Jun oth Tao, Lei oth Qian, Kun oth Ma, Pengcheng oth Enthalten in Elsevier López-Gopar, Mario E. ELSEVIER Mexican student-teachers’ “English” language praxicum: Decolonizing attempts 2022 EJP New York, NY [u.a.] (DE-627)ELV008405875 volume:851 year:2019 day:15 month:05 pages:174-185 extent:12 https://doi.org/10.1016/j.ejphar.2019.03.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 851 2019 15 0515 174-185 12 |
| allfieldsGer |
10.1016/j.ejphar.2019.03.004 doi GBV00000000000572.pica (DE-627)ELV046301844 (ELSEVIER)S0014-2999(19)30153-0 DE-627 ger DE-627 rakwb eng 370 VZ 5,3 ssgn Li, Hongyang verfasserin aut Adapalene suppressed the proliferation of melanoma cells by S-phase arrest and subsequent apoptosis via induction of DNA damage 2019transfer abstract 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Malignant melanoma was the leading cause of mortality among the skin-associated cancer owing to its highly metastatic feature, increasing incidence and drug resistance requirement. Retinoids played important roles in the treatment of cancer via the activation of retinoid acid receptor (RAR) or retinoid X receptor (RXR). Our present study showed that the third-generation retinoid adapalene exhibited strong inhibitory effects on the proliferation of melanoma cells than other retinoids, such as all-trans-retinoic acid (ATRA), isotretinoin, acitretin and bexarotene, and adapalene exerted significant inhibitory effects on the colony formation of melanoma cells. Further study confirmed that adapalene treatment triggered dramatic S phase arrest and apoptosis, and S phase arrest was the potential mechanism of apoptosis induction. In addition, adapalene treatment dramatically regulated the expression of S phase-related protein, and increased the protein level of DNA damage marker，which were consistent with the results of the induction of the tail moment in comet assays. Meanwhile, DNA damage response was activated and the DNA repair pathway was simultaneously inhibited by adapalene treatment, which might furtherly potentiate S phase arrest and subsequent apoptosis. Taken together, these results showed that adapalene exhibited strong anti-cancer activity, and might be a candidate agent for the clinical treatment of melanoma. Malignant melanoma was the leading cause of mortality among the skin-associated cancer owing to its highly metastatic feature, increasing incidence and drug resistance requirement. Retinoids played important roles in the treatment of cancer via the activation of retinoid acid receptor (RAR) or retinoid X receptor (RXR). Our present study showed that the third-generation retinoid adapalene exhibited strong inhibitory effects on the proliferation of melanoma cells than other retinoids, such as all-trans-retinoic acid (ATRA), isotretinoin, acitretin and bexarotene, and adapalene exerted significant inhibitory effects on the colony formation of melanoma cells. Further study confirmed that adapalene treatment triggered dramatic S phase arrest and apoptosis, and S phase arrest was the potential mechanism of apoptosis induction. In addition, adapalene treatment dramatically regulated the expression of S phase-related protein, and increased the protein level of DNA damage marker，which were consistent with the results of the induction of the tail moment in comet assays. Meanwhile, DNA damage response was activated and the DNA repair pathway was simultaneously inhibited by adapalene treatment, which might furtherly potentiate S phase arrest and subsequent apoptosis. Taken together, these results showed that adapalene exhibited strong anti-cancer activity, and might be a candidate agent for the clinical treatment of melanoma. Bexarotene (PubChem CID: 82146) Elsevier ATRA (PubChem CID: 444795) Elsevier Adapalene (PubChem CID: 60164) Elsevier Isotretinoin (PubChem CID: 5282379) Elsevier Acitretin (PubChem CID: 5284513) Elsevier Wang, Cheng oth Li, Lingjun oth Bu, Wenbo oth Zhang, Mengli oth Wei, Jun oth Tao, Lei oth Qian, Kun oth Ma, Pengcheng oth Enthalten in Elsevier López-Gopar, Mario E. ELSEVIER Mexican student-teachers’ “English” language praxicum: Decolonizing attempts 2022 EJP New York, NY [u.a.] (DE-627)ELV008405875 volume:851 year:2019 day:15 month:05 pages:174-185 extent:12 https://doi.org/10.1016/j.ejphar.2019.03.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 851 2019 15 0515 174-185 12 |
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10.1016/j.ejphar.2019.03.004 doi GBV00000000000572.pica (DE-627)ELV046301844 (ELSEVIER)S0014-2999(19)30153-0 DE-627 ger DE-627 rakwb eng 370 VZ 5,3 ssgn Li, Hongyang verfasserin aut Adapalene suppressed the proliferation of melanoma cells by S-phase arrest and subsequent apoptosis via induction of DNA damage 2019transfer abstract 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Malignant melanoma was the leading cause of mortality among the skin-associated cancer owing to its highly metastatic feature, increasing incidence and drug resistance requirement. Retinoids played important roles in the treatment of cancer via the activation of retinoid acid receptor (RAR) or retinoid X receptor (RXR). Our present study showed that the third-generation retinoid adapalene exhibited strong inhibitory effects on the proliferation of melanoma cells than other retinoids, such as all-trans-retinoic acid (ATRA), isotretinoin, acitretin and bexarotene, and adapalene exerted significant inhibitory effects on the colony formation of melanoma cells. Further study confirmed that adapalene treatment triggered dramatic S phase arrest and apoptosis, and S phase arrest was the potential mechanism of apoptosis induction. In addition, adapalene treatment dramatically regulated the expression of S phase-related protein, and increased the protein level of DNA damage marker，which were consistent with the results of the induction of the tail moment in comet assays. Meanwhile, DNA damage response was activated and the DNA repair pathway was simultaneously inhibited by adapalene treatment, which might furtherly potentiate S phase arrest and subsequent apoptosis. Taken together, these results showed that adapalene exhibited strong anti-cancer activity, and might be a candidate agent for the clinical treatment of melanoma. Malignant melanoma was the leading cause of mortality among the skin-associated cancer owing to its highly metastatic feature, increasing incidence and drug resistance requirement. Retinoids played important roles in the treatment of cancer via the activation of retinoid acid receptor (RAR) or retinoid X receptor (RXR). Our present study showed that the third-generation retinoid adapalene exhibited strong inhibitory effects on the proliferation of melanoma cells than other retinoids, such as all-trans-retinoic acid (ATRA), isotretinoin, acitretin and bexarotene, and adapalene exerted significant inhibitory effects on the colony formation of melanoma cells. Further study confirmed that adapalene treatment triggered dramatic S phase arrest and apoptosis, and S phase arrest was the potential mechanism of apoptosis induction. In addition, adapalene treatment dramatically regulated the expression of S phase-related protein, and increased the protein level of DNA damage marker，which were consistent with the results of the induction of the tail moment in comet assays. Meanwhile, DNA damage response was activated and the DNA repair pathway was simultaneously inhibited by adapalene treatment, which might furtherly potentiate S phase arrest and subsequent apoptosis. Taken together, these results showed that adapalene exhibited strong anti-cancer activity, and might be a candidate agent for the clinical treatment of melanoma. Bexarotene (PubChem CID: 82146) Elsevier ATRA (PubChem CID: 444795) Elsevier Adapalene (PubChem CID: 60164) Elsevier Isotretinoin (PubChem CID: 5282379) Elsevier Acitretin (PubChem CID: 5284513) Elsevier Wang, Cheng oth Li, Lingjun oth Bu, Wenbo oth Zhang, Mengli oth Wei, Jun oth Tao, Lei oth Qian, Kun oth Ma, Pengcheng oth Enthalten in Elsevier López-Gopar, Mario E. ELSEVIER Mexican student-teachers’ “English” language praxicum: Decolonizing attempts 2022 EJP New York, NY [u.a.] (DE-627)ELV008405875 volume:851 year:2019 day:15 month:05 pages:174-185 extent:12 https://doi.org/10.1016/j.ejphar.2019.03.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 851 2019 15 0515 174-185 12 |
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Li, Hongyang ddc 370 ssgn 5,3 Elsevier Bexarotene (PubChem CID: 82146) Elsevier ATRA (PubChem CID: 444795) Elsevier Adapalene (PubChem CID: 60164) Elsevier Isotretinoin (PubChem CID: 5282379) Elsevier Acitretin (PubChem CID: 5284513) Adapalene suppressed the proliferation of melanoma cells by S-phase arrest and subsequent apoptosis via induction of DNA damage |
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adapalene suppressed the proliferation of melanoma cells by s-phase arrest and subsequent apoptosis via induction of dna damage |
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Adapalene suppressed the proliferation of melanoma cells by S-phase arrest and subsequent apoptosis via induction of DNA damage |
| abstract |
Malignant melanoma was the leading cause of mortality among the skin-associated cancer owing to its highly metastatic feature, increasing incidence and drug resistance requirement. Retinoids played important roles in the treatment of cancer via the activation of retinoid acid receptor (RAR) or retinoid X receptor (RXR). Our present study showed that the third-generation retinoid adapalene exhibited strong inhibitory effects on the proliferation of melanoma cells than other retinoids, such as all-trans-retinoic acid (ATRA), isotretinoin, acitretin and bexarotene, and adapalene exerted significant inhibitory effects on the colony formation of melanoma cells. Further study confirmed that adapalene treatment triggered dramatic S phase arrest and apoptosis, and S phase arrest was the potential mechanism of apoptosis induction. In addition, adapalene treatment dramatically regulated the expression of S phase-related protein, and increased the protein level of DNA damage marker，which were consistent with the results of the induction of the tail moment in comet assays. Meanwhile, DNA damage response was activated and the DNA repair pathway was simultaneously inhibited by adapalene treatment, which might furtherly potentiate S phase arrest and subsequent apoptosis. Taken together, these results showed that adapalene exhibited strong anti-cancer activity, and might be a candidate agent for the clinical treatment of melanoma. |
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Malignant melanoma was the leading cause of mortality among the skin-associated cancer owing to its highly metastatic feature, increasing incidence and drug resistance requirement. Retinoids played important roles in the treatment of cancer via the activation of retinoid acid receptor (RAR) or retinoid X receptor (RXR). Our present study showed that the third-generation retinoid adapalene exhibited strong inhibitory effects on the proliferation of melanoma cells than other retinoids, such as all-trans-retinoic acid (ATRA), isotretinoin, acitretin and bexarotene, and adapalene exerted significant inhibitory effects on the colony formation of melanoma cells. Further study confirmed that adapalene treatment triggered dramatic S phase arrest and apoptosis, and S phase arrest was the potential mechanism of apoptosis induction. In addition, adapalene treatment dramatically regulated the expression of S phase-related protein, and increased the protein level of DNA damage marker，which were consistent with the results of the induction of the tail moment in comet assays. Meanwhile, DNA damage response was activated and the DNA repair pathway was simultaneously inhibited by adapalene treatment, which might furtherly potentiate S phase arrest and subsequent apoptosis. Taken together, these results showed that adapalene exhibited strong anti-cancer activity, and might be a candidate agent for the clinical treatment of melanoma. |
| abstract_unstemmed |
Malignant melanoma was the leading cause of mortality among the skin-associated cancer owing to its highly metastatic feature, increasing incidence and drug resistance requirement. Retinoids played important roles in the treatment of cancer via the activation of retinoid acid receptor (RAR) or retinoid X receptor (RXR). Our present study showed that the third-generation retinoid adapalene exhibited strong inhibitory effects on the proliferation of melanoma cells than other retinoids, such as all-trans-retinoic acid (ATRA), isotretinoin, acitretin and bexarotene, and adapalene exerted significant inhibitory effects on the colony formation of melanoma cells. Further study confirmed that adapalene treatment triggered dramatic S phase arrest and apoptosis, and S phase arrest was the potential mechanism of apoptosis induction. In addition, adapalene treatment dramatically regulated the expression of S phase-related protein, and increased the protein level of DNA damage marker，which were consistent with the results of the induction of the tail moment in comet assays. Meanwhile, DNA damage response was activated and the DNA repair pathway was simultaneously inhibited by adapalene treatment, which might furtherly potentiate S phase arrest and subsequent apoptosis. Taken together, these results showed that adapalene exhibited strong anti-cancer activity, and might be a candidate agent for the clinical treatment of melanoma. |
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