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the present study demonstrates that miR-422a may serve as a tumor suppressor in osteosarcoma via inhibiting BCL2L2 and KRAS translation both in vitro and in vivo Therefore, miR-422a could be developed as a novel therapeutic target in osteosarcoma.
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BCL2L2 knockdown was attenuated the effects of SNHG1 overexpression on cell viability, cell apoptosis and protein levels of cleaved caspase-3, cleaved caspase-9 and Bax in H2O2-treated human cardiomyocytes.
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Our comprehensive analysis indicates B-cell lymphomas commonly select for BCLW overexpression in combination with or instead of other antiapoptotic BCL2 family members.
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BCL-W contributes to the threshold of anti-apoptotic activity during mitosis
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we demonstrated that miR-126-5p plays an inhibitory role in human cervical cancer progression, regulating the apoptosis of cancer cells via directly targeting Bcl2l2.
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High expression of Bcl-w was associated with mesenchymal changes and invading populations in the glioblastoma multiforme; Bcl-w functions as a positive regulator of invasion by enhancing mesenchymal traits of glioblastoma multiforme, consequently contributing to malignancy.
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BCL2L2 was the virtual target of miR-133b, and we found a negative regulatory relationship between miR-133b and BCL2L2. MiR-133b and BCL2L2 interfered with the viability and apoptosis of cells.
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overexpression of miR-15a in the FaDu cells was associated with significantly decreased BCL2L2 and BCL2 expression and a significant increase in the apoptosis rate. The opposite results were observed in HPV-positive HSCC, where downregulation of miR-15a suppressed apoptosis
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we conclude that BER treatment reduces cisplatin resistance of gastric cancer cells by modulating the miR-203/Bcl-w apoptotic axis. BER may be a novel agent to enhance chemotherapeutic responses in cisplatin-resistant gastric cancer patients
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Genetic and pharmacological inhibition of BCL-W and BCL-XL causes directed elimination of senescent cells.
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Data show that BCL2-like 2 protein (BCL2L2) is a direct target of micrRNA miR-29b.
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these results indicate that miR-335 acts as a novel tumor suppressor to regulate ccRCC cell proliferation and invasion through downregulation of BCL-W expression.
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miR-15a acts as a tumor suppressor in NSCLC by directly targeting BCL2L2 and may serve as a potential diagnostic biomarker and therapeutic target for NSCLC.
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The crystal structures of BCL-W and BCL-XL, along with cellular, studies reveal critical features of the BH3 domains of pro-survival proteins that distinguish them functionally from their pro-apoptotic counterparts.
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over-expression of miR-195 sensitized resistant cells to DOX and enhanced cell apoptosis activity, all of which can be partly rescued by BCL2L2 siRNA and cDNA expression
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A structural basis for a conserved binding mechanism between p53DBD and the anti-apoptotic Bcl-2 family proteins.
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Bcl-w-induced Sp1 activation is a potential marker for aggressiveness of glioblastoma multiforme.
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HDMF inhibits Bcl-w-induced neurosphere formation and the expression of glioma stem cell markers, such as Musashi, Sox-2 and c-myc.
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Crystal structure of human BCL-W in complex with different DARPins is virtually identical to the ligand-free conformation of its closest relative BCL-XL.
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MiR-335 lacks of expression brings about the abnormal accumulation of Bcl-w.
