Evidence for upregulation of BIM and the splicing factor SRp55 in melanoma cells from patients treated with selective BRAF inhibitors Running Head: Induction of apoptosis in melanoma by BRAF inhibitors
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Immunohistochemical Investigation of Mutant BRAF V600E in Common Pigmented Skin Neoplasms, Study on a Sample of Iranian Patients
Background & Objective: This study was designed for the first time for the detection of mutant BRAF V600E and its correlation with clinicophathologic features in a sample of Iranian patients with pathologically proved pigmented skin neoplasms.Methods: 82 paraffin-embedded blocks, including melanocytic nevi, malignant melanoma, Basel cell carcinoma, and sq...
متن کاملCombining BET and HDAC inhibitors synergistically induces apoptosis of melanoma and suppresses AKT and YAP signaling
Histone acetylation marks have an important role in controlling gene expression and are removed by histone deacetylases (HDACs). These marks are read by bromodomain and extra-terminal (BET) proteins and novel inhibitiors of these proteins are currently in clinical development. Inhibitors of HDAC and BET proteins have individually been shown to cause apoptosis and reduce growth of melanoma cells...
متن کاملOverexpression of Mcl-1 confers resistance to BRAFV600E inhibitors alone and in combination with MEK1/2 inhibitors in melanoma.
Melanoma harboring BRAF mutations frequently develop resistance to BRAF inhibitors, limiting the impact of treatment. Here, we establish a mechanism of resistance and subsequently identified a suitable drug combination to overcome the resistance. Single treatment of BRAF mutant melanoma cell lines with vemurafenib or dabrafenib (BRAF inhibitors) alone or in combination with trametinib (MEK1/2 i...
متن کاملMitochondrial ATF2 translocation contributes to apoptosis induction and BRAF inhibitor resistance in melanoma through the interaction of Bim with VDAC1
BACKGROUND The mitochondrial accumulation of ATF2 is involved in tumor suppressor activities via cytochrome c release in melanoma cells. However, the signaling pathways that connect mitochondrial ATF2 accumulation and cytochrome c release are not well documented. METHODS Several melanoma cell lines, B16F10, K1735M2, A375 and A375-R1, were treated with paclitaxel and vemurafenib to test the fu...
متن کاملThe c-Jun/RHOB/AKT pathway confers resistance of BRAF-mutant melanoma cells to MAPK inhibitors
The response of BRAF-mutant melanoma patients to BRAF inhibitors is dramatically impaired by secondary resistances and rapid relapse. So far, the molecular mechanisms driving these resistances are not completely understood. Here, we show that, in BRAF-mutant melanoma cells, inhibition of BRAF or its target MEK induces RHOB expression by a mechanism that depends on the transcription factor c-Jun...
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تاریخ انتشار 2014