RNA-binding motif protein 5 negatively regulates the activity of Wnt/β-catenin signaling in cigarette smoke-induced alveolar epithelial injury

Hao, Yuqiu; Su, Zheng; Lv, Xuejiao; Li, Ping; Gao, Peng; Wang, Chen; Bai, Yinjuan; Zhang, Jie

doi:10.3892/or.2015.3828

Cited by 13 publications

(14 citation statements)

References 26 publications

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“…Also, it was shown to inhibit canonical Wnt/β-catenin signaling [14]. So, we determined the critical molecules in both apoptosis and Wnt/β-catenin signaling pathway.…”

Section: Resultsmentioning

confidence: 99%

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RBM5 inhibits tumorigenesis of gliomas through inhibition of Wnt/β-catenin signaling and induction of apoptosis

et al. 2017

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BackgroundGliomas are one of the most common malignant brain tumors and bring a big threat to human life as traditional therapy is unsatisfactory. RBM5 was a RNA-binding motif protein and was reported as a tumor suppressor. But the role of RBM5 in gliomas was unknown.MethodsThe mRNA level of RBM5 was determined in gliomas tissues and cell lines by real-time quantitative PCR (qRT-PCR) assay while the association of RBM5 expression with prognosis was analyzed by Kaplan-Meier method and compared by log-rank test. Lentivirus was used to overexpress RBM5 in gliomas cells. MTT and BrdU incorporation assay were used to determine cell proliferation and DNA synthesis when the ability of cell migration and invasion was analyzed by transwell assay with/without Matrigel. Cell apoptosis rate was determined with fluorescence-activated cell sorting (FACS) method. Then, expression of apoptosis molecules and critical members in Wnt/β-catenin pathway were detected by western blot analysis.ResultsRBM5 was shown to be downregulated in gliomas tissues and gliomas cell lines. And decreased RBM5 expression was clinically correlated with tumor stage, patient age, and poor prognosis of gliomas patients. The proliferation and DNA synthesis was dramatically inhibited when RBM5 was overexpressed in SHG44 or U251 cells. Also, the ability of cell migration and invasion was disrupted. Then, the level of β-catenin and Cyclin D1 significantly decreased when DKK1 and P-GSK-3β increased reversely in SHG44 cells, which suggested that RBM5 inhibited canonical Wnt/β-catenin signaling. Meanwhile, we demonstrated that caspase3-mediated apoptotic pathway was activated by RBM5 as Bax, TNF-α, and cleaved caspase3 were greatly upregulated while antiapoptotic molecule Bcl-2 was downregulated. Additionally, that apoptotic rate increased significantly from less than 1 to 32% in RBM5-overexpressed SHG44 cells further supported the pro-apoptosis role of RBM5 in gliomas cells.ConclusionsRBM5 plays a suppressor role in human gliomas by inhibiting Wnt/β-catenin signaling and inducing cell apoptosis. This study improves our knowledge about the carcinogenesis and progression of human gliomas, which would greatly contribute to the therapy for gliomas patients.

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“…Also, it was shown to inhibit canonical Wnt/β-catenin signaling [14]. So, we determined the critical molecules in both apoptosis and Wnt/β-catenin signaling pathway.…”

Section: Resultsmentioning

confidence: 99%

“…In early research, RBM5 was reported to regulate the splicing of an apoptotic factor Fas and resensitize lung cancer cells A549 to cisplatin [13]. Also, RBM5 was shown to inhibit Wnt/β-catenin signaling in A549 cells [14]. Wnt/β-catenin signaling was vital to cancer cell proliferation.…”

Section: Introductionmentioning

confidence: 99%

RBM5 inhibits tumorigenesis of gliomas through inhibition of Wnt/β-catenin signaling and induction of apoptosis

et al. 2017

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“…RBM5-mediated apoptosis is associated with up-regulation of the proapoptotic protein B-cell leukemia/lymphoma 2-associated X, downregulation of the antiapoptotic proteins B-cell leukemia/ lymphoma 2 and B-cell leukemia/lymphoma 2-like 1, increased release of mitochondrial cytochrome c into the cytosol, and increased activation of caspases 9 and 3 (13,38,51). Previous research has shown that the overexpression of RBM5 inhibited canonical Wnt-b-catenin signaling and regulated cell apoptosis (14,15). However, the role of RBM5 in BUC remains unexplored.…”

Section: Discussionmentioning

confidence: 99%

“…RBM5 was most frequently reported to induce apoptosis by regulating caspase-2 and Fas alternative splicing (6,17). Furthermore, it was shown to inhibit canonical Wnt-bcatenin signaling (14,15). Consequently, we determined the critical molecules involved in both the apoptosis and Wnt-b-catenin signaling pathways.…”

Section: Rbm5 Induces Bladder-cell Apoptosis By Depressing B-catenin mentioning

confidence: 99%

“…The overexpression of RBM5 in various cell lines led to growth arrest, induction of apoptosis, and retarded tumor growth in nude mice (11)(12)(13). Also, RBM5 was shown to inhibit Wnt-b-catenin signaling and promote A549 cell apoptosis (14,15). Recently, some studies indicated that RBM5 regulates the alternative splicing of Fas and caspase-2 precursor mRNA by interfering with splice-site pairing (6,16,17).…”

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Down‐regulated RBM5 inhibits bladder cancer cell apoptosis by initiating an miR‐432‐5p/β‐catenin feedback loop

et al. 2019

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RNA‐binding motif protein 5 (RBM5) acts as a tumor suppressor in various human cancers and presents with several important characteristics, such as the potentiation of apoptosis, inhibition of the cell cycle, and alternative splicing of Fas and caspase‐2 precursor mRNA. However, its role in bladder urothelial carcinoma (BUC) remains unknown. In this study, we found that RBM5 expression was significantly down‐regulated in BUC tissues when compared with the adjacent nontumor tissues. The down‐regulation of RBM5 activates ²‐catenin, which binds to the T‐cell factor/lymphocyte enhancer factor element of the miR‐432‐5p promoter and elevates the expression of miR‐432‐5p in bladder cancer cells. The up‐regulated miR‐432‐5p directly targets 3′‐UTR and depresses RBM5 expression. Thus, RBM5–miR‐432‐5p–²‐catenin forms a feedback loop in regulating bladder cancer cell apoptosis. Our findings provide evidence that the regulatory feedback loop among RBM5, miR‐432‐5p, and Wnt–²‐catenin is responsible for the progress of bladder cancer cells.—Zhang, Y.‐P., Liu, K.‐L., Wang, Y.‐X., Yang, Z., Han, Z.‐W., Lu, B.‐S., Qi, J.‐C, Yin, Y.‐W., Teng, Z.‐H., Chang, X.‐L., Li, J.‐D., Xin, H., Li, W. Down‐regulated RBM5 inhibits bladder cancer cell apoptosis by initiating an miR‐432‐5p/²‐catenin feedback loop. FASEB J. 33, 10973–10985 (2019). http://www.fasebj.org

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RNA-binding Proteins as a New Link Between COPD and Lung Cancer

Nucera

Salvato

Ricciardi

et al. 2023

Interdisciplinary Cancer Research

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RNA-binding motif protein 5 negatively regulates the activity of Wnt/β-catenin signaling in cigarette smoke-induced alveolar epithelial injury

Cited by 13 publications

References 26 publications

RBM5 inhibits tumorigenesis of gliomas through inhibition of Wnt/β-catenin signaling and induction of apoptosis

RBM5 inhibits tumorigenesis of gliomas through inhibition of Wnt/β-catenin signaling and induction of apoptosis

Down‐regulated RBM5 inhibits bladder cancer cell apoptosis by initiating an miR‐432‐5p/β‐catenin feedback loop

RNA-binding Proteins as a New Link Between COPD and Lung Cancer

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