Long non‑coding RNA AC245100.4 promotes prostate cancer tumorigenesis via the microRNA‑145‑5p/RBBP5 axis

Xie, Hui; Zhao, Jiabin; Wan, Jiahui; Zhao, Jianzhou; Wang, Qianqian; Yang, Xu; Yang, Weiyu; Lin, Ping; Yu, Xiuchong

doi:10.3892/or.2020.7894

Cited by 17 publications

(16 citation statements)

References 40 publications

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“…There is increasing evidence that the ceRNA regulatory network plays a role in cancer development and occurrence [12][13][14]. It might be possible to uncover the mechanism by which CASC1 influences bladder cancer progression by studying the ceRNA network.…”

Section: Introductionmentioning

confidence: 99%

CASC1 Expression in Bladder Cancer Is Regulated by Exosomal miRNA-150: A Comprehensive Pan-Cancer and Bioinformatics Study

Luo

et al. 2022

Computational and Mathematical Methods in Medicine

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This study explored the role of cancer susceptibility 1 (CASC1) in tumorigenesis and development as well as the key pathways affecting bladder cancer progression. CASC1 was examined in various normal tissues in humans using the HPA database to quantify its expression level and subcellular localization. CASC1 is abundantly expressed in tumor tissues, primarily in cytoplasmic vesicles and stroma. TIMER2 was used to analyze the correlation between CASC1 expression levels and the types of infiltrates associated with immune cells and immunosuppressive cells. MDSC, Treg, M2, and CAF were significantly correlated with CASC1 expression in various tumors. Comparing patients with and without CASC1 mutation, those with CASC1 mutation had worse overall survival, progression-free survival, and disease-free survival. The correlation between has-miR-150 and CASC1 (for the case of bladder cancer) was then analyzed, and the related ceRNA network was mapped. A negative relationship between CASC1 expression and has-miR-150 expression was found in cases of bladder cancer. And the presence of miR-150-targeted CASC1 may be associated with bladder cancer progression. CASC1 is expressed at elevated levels in various tumor tissues, and it is associated with tumorigenesis and development. Exosomes containing miR-150-targeted CASC1 may affect the progression of bladder cancer.

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Section: Introductionmentioning

confidence: 99%

CASC1 Expression in Bladder Cancer Is Regulated by Exosomal miRNA-150: A Comprehensive Pan-Cancer and Bioinformatics Study

Luo

et al. 2022

Computational and Mathematical Methods in Medicine

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“…In association with ASH2L and WDR5, RBBP5 stimulates the histone methyltransferase activities of KMT2A, KMT2B, KMT2C, KMT2D, SETD1A and SETD1B (Avdic, et al 2011. Studies have shown that RBBP5 is associated with many cancers (Xie, et al 2021, Zhou, et al 2018, Zhao, et al 2015, such as prostate cancer (Xie, et al 2021), hepatocellular carcinoma (Zhou, et al 2018) and gliomas (Zhao, et al 2015). These results indicate that the expression of RBBP5 was upregulated and played a crucial role in the progression of tumours.…”

Section: Discussionmentioning

confidence: 93%

“…Therefore, the deletion of RBBP5 may lead to a decrease in H3K4 methyltransferase activity and the degree of H3K4 methylation. In addition, previous studies have shown that RBBP5 is associated with prostate carcinoma (Xie, et al 2021), hepatocellular carcinoma (Zhou, et al 2018), multiple myeloma ), gliomas (Zhao, et al 2015), etc.…”

Section: Introductionmentioning

confidence: 97%

Retinoblastoma-binding protein 5 regulates H3K4 methylation modification to inhibit the proliferation of melanoma cells by inactivating the Wnt/β-catenin and epithelial-mesenchymal transition pathways

Yang

Jia

Wang

et al. 2022

Preprint

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Background Histone 3 lysine 4 methylation (H3K4me), especially histone 3 lysine 4 trimethylation (H3K4me3), is one of the most extensively studied patterns of histone modification and plays crucial roles in many biological processes. However, as a part of H3K4 methyltransferase that participates in H3K4 methylation and transcriptional regulation, retinoblastoma-binding protein 5 (RBBP5) has not been well studied in melanoma cancer. The present study sought to explore RBBP5-mediated H3K4 histone modification and the potential mechanisms in melanoma. Methods RBBP5 expression in melanoma and nevi specimens was detected by immunohistochemistry. Western blotting was performed for three pairs of melanoma cancer tissues and nevi tissues. In vitro and in vivo assays were used to investigate the function of RBBP5. The molecular mechanism was determined using RT-qPCR, western blotting, ChIP assays, and co-IP assays. Results Our study showed that RBBP5 was significantly downregulated in melanoma tissue and cells compared with nevi tissues and normal epithelia cells (P < 0.05). Reducing RBBP5 in human melanoma cells leads to H3K4me3 downregulation and promotes cell proliferation, migration, and invasion. On the one hand, we verified that WD repeat and SOCS box containing protein 2(WSB2) was an upstream gene of RBBP5-mediated H3K4 modification, which could directly bind to RBBP5 and negatively regulate its expression. On the other hand, we also confirmed that p16 (a cancer suppressor gene), was a downstream target of H3K4me3, the promoter of which can directly bind to H3K4me3. Mechanistically, our data revealed that RBBP5 inactivated the Wnt/β-catenin and epithelial-mesenchymal transition (EMT) pathways (P < 0.05), leading to melanoma suppression. Conclusion Histone methylation is rising as an important factor affecting tumorigenicity and tumour progression. Our findings verified the significance of RBBP5-mediated H3K4 modification in melanoma and the potential regulatory mechanisms of melanoma proliferation and growth, suggesting that RBBP5 is a potential therapeutic target for the treatment of melanoma.

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“…Our previous reports indicated that long non‐coding RNA AC245100.4 is markedly upregulated in PCa tissues and cells (Cui et al, 2020). Interference by AC245100.4 was shown to significantly inhibit PCa progression (Xie et al, 2021). The results of next‐generation sequencing (NGS) technology showed that 117 genes were upregulated after silencing of AC245100.4, including APIP .…”

Section: Discussionmentioning

confidence: 99%

Apaf‐1 interacting protein, a new target of microRNA‐146a‐3p, promotes prostate cancer cell development via the ERK1/2 pathway

Wang

Jia

et al. 2022

Cell Biology International

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The Apaf‐1 interacting protein (APIP), a ubiquitously expressed antiapoptotic molecule, is aberrantly expressed and of great significance in various cancers. However, little is known regarding the potential value and underlying mechanisms of APIP in prostate cancer. Here, we demonstrated that APIP expression is significantly upregulated in prostate cancer cell lines. APIP overexpression promoted tumor cell proliferation and migration and induced extracellular regulated protein kinases 1/2 (ERK1/2) activation. Pharmacological inhibition of ERK1/2 signaling reversed APIP‐induced increase in cell proliferation and migration induced by APIP overexpression. Expression of APIP was hampered by miR‐146a‐3p. A dual luciferase reporter gene assay identified the regulatory relationship between APIP and miR‐146a‐3p in prostate cancer, suggesting that APIP is a direct target of miR‐146a‐3p. miR‐146a‐3p reduced cell proliferation and migration in prostate cancer. Furthermore, miR‐146a‐3p inhibited ERK1/2 activation. Application of an ERK1/2 inhibitor reversed the increase in cell proliferation and migration induced by miR‐146a‐3p inhibition. In summary, this study focused on the role of APIP in regulating cell growth and migration and proposes a theoretical basis for APIP as a promising biomarker in prostate cancer development.

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Long non‑coding RNA AC245100.4 promotes prostate cancer tumorigenesis via the microRNA‑145‑5p/RBBP5 axis

Cited by 17 publications

References 40 publications

CASC1 Expression in Bladder Cancer Is Regulated by Exosomal miRNA-150: A Comprehensive Pan-Cancer and Bioinformatics Study

CASC1 Expression in Bladder Cancer Is Regulated by Exosomal miRNA-150: A Comprehensive Pan-Cancer and Bioinformatics Study

Retinoblastoma-binding protein 5 regulates H3K4 methylation modification to inhibit the proliferation of melanoma cells by inactivating the Wnt/β-catenin and epithelial-mesenchymal transition pathways

Apaf‐1 interacting protein, a new target of microRNA‐146a‐3p, promotes prostate cancer cell development via the ERK1/2 pathway

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