MiR-30a-5p frequently downregulated in prostate cancer inhibits cell proliferation via targeting PCLAF

Hu, Zhao; Lai, Xiaofeng; Zhang, Wei; Zhu, Honglin; Zhang, Shenhang; Wu, Wei; Wang, Shuiliang; Tang, Min-ying; Deng, Zhen; Tan, Jianming

doi:10.1080/21691401.2018.1553783

Cited by 31 publications

(34 citation statements)

References 41 publications

(36 reference statements)

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“…miR‐30a has been shown to play an inhibitory role in many cancers, such as cancers of the colon, breast, and lung 38‐40 . miR‐30a has also been previously reported to function as a tumor suppressor in PCa 12,13,15,16,41 . miR‐30a inhibits proliferation, 15,16 invasion and epithelial‐mesenchymal transition of PCa cells 12,41 .…”

Section: Discussionmentioning

confidence: 97%

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miR‐30a inhibits androgen‐independent growth of prostate cancer via targeting MYBL2, FOXD1, and SOX4

et al. 2020

The Prostate

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Background: Castrate-resistant prostate cancer (CRPC) is an aggressive and lethal disease. The pathogenesis of CRPC is not fully understood and novel therapeutic targets need to be identified to improve the patients' prognosis. has been demonstrated to be a tumor suppressor in many types of solid malignancies. However, its role in androgen-independent (AI) growth of prostate cancer (PCa) received limited attention as yet. Methods:The clinical association of miR-30a and its potential targets with AI growth was characterized by bioinformatics analyses. Regulation of cell proliferation and colony formation rates by miR-30a were tested using PCa cell models. Xenograft models were used to measure the regulation of prostate tumor growth by miR-30a.The real-time quantitative polymerase chain reaction was used to validate whether miR-30a and its targets regulate cell cycle control genes and androgen receptor (AR)-dependent transcription. Bioinformatics tools, Western blot, and luciferase reporter assays were utilized to identify miR-30a targets. Results: Bioinformatic analysis showed that low expression of miR-30a is associated with castration resistance of PCa patients and poor outcomes. Transfection of miR-30a mimics inhibited the AI growth of PCa cells in vitro and in vivo. Upregulation of miR-30a in 22RV1 cells altered the expression of cell cycle control genes and AR-mediated transcription, while downregulation of miR-30a in LNCaP cells had the opposite effects to AR-mediated transcription. MYBL2, FOXD1, and SOX4 were identified as miR-30a targets. Downregulation of MYBL2, FOXD1, and SOX4 affected the expression of cell cycle control genes and AR-mediated transcription and suppressed the AI growth of 22RV1 cells. Conclusions: Our results suggest that miR-30a inhibits AI growth of PCa by targeting MYBL2, FOXD1, and SOX4. They provide novel insights into developing new treatment strategies for CRPC. K E Y W O R D S castration-resistant prostate cancer, FOXD1, miR-30a, MYBL2, SOX4

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Section: Discussionmentioning

confidence: 97%

“…Previously, we and others have shown that the aberrant expression of miR‐30a is associated with epithelial‐mesenchymal transition, radiosensitivity, proliferation, and invasion in PCa 12‐16 . To the best of our knowledge, the role of miR‐30a in CRPC has not been fully elucidated.…”

Section: Introductionmentioning

confidence: 93%

miR‐30a inhibits androgen‐independent growth of prostate cancer via targeting MYBL2, FOXD1, and SOX4

et al. 2020

The Prostate

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“…Currently, the expression profile and function of miR-30a-5p in different malignancies are still existed controversies. A large number of reports have demonstrated that miR-30a-5p was commonly down-expression and regulated biological behaviors of tumor growth, invasion, epithelial-mesenchymal transition (EMT) in various types of cancers [13,14,18]. miR-30a-5p was down-regulated in prostate cancer and inhibited cell proliferation via targeting PCLAF [14].…”

Section: Discussionmentioning

confidence: 99%

“…A large number of reports have demonstrated that miR-30a-5p was commonly down-expression and regulated biological behaviors of tumor growth, invasion, epithelial-mesenchymal transition (EMT) in various types of cancers [13,14,18]. miR-30a-5p was down-regulated in prostate cancer and inhibited cell proliferation via targeting PCLAF [14]. Furthermore, the down-regulation of miR-30a-5p was associated with poor prognosis and promoted chemoresistance of gemcitabine in pancreatic ductal adenocarcinoma [19].…”

Section: Discussionmentioning

confidence: 99%

“…The miR-30 family, which contains five members of distinct pre-mature miRNAs (miR-30a, -30b, -30c, -30d, -30e), has been proved to play diverse roles in regulating essential aspects of tumorigenesis, metastasis, chemo-resistance and clinical prognosis in several types of human cancers [11,12]. A large number of reports have demonstrated that miR-30a-5p, as a member of the mir-30 family, was down-regulated and associated with tumorigenesis and progression of prostate cancer, hepatocellular carcinoma, breast tumor and some other cancers [13][14][15]. However, it has been reported that overexpression of miR-30a-5p contributed to initiation and progression of some tumors [12,16].…”

Section: Ivyspring International Publishermentioning

confidence: 99%

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MiR-30a-5p promotes cholangiocarcinoma cell proliferation through targeting SOCS3

Zhang¹,

Wang²,

Li³

et al. 2020

J. Cancer

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Background: MicroRNAs (miRNAs) play important roles in the occurrence and development of cancers. In this project, we aimed to explore the role and molecular mechanism of mir-30a-5p in cholangiocarcinoma (CCA). Materials and Methods:The expression profile and clinical significance of miR-30a-5p in CCA patients were investigated in 31 ICC and 52 ECC patients respectively. The role and mechanism of miR-30a-5p in CCA cells were investigated by up-regulating and inhibiting miR-30a-5p expression in vitro functional study. Results: The expression of miR-30a-5p was increased in both CCA tissues and cells. The inhibition of miR-30a-5p decreased cell proliferation and induced cell apoptosis while overexpression of miR-30a-5p achieved the opposite effect. Furthermore, SOCS3 was down-regulated in ICC and ECC tissues and negatively regulated by miR-30a-5p. Dual-luciferase reporter assay revealed that co-transfection of miR-30a-5p significantly inhibited the activity of firefly luciferase reporter carrying the wild-type 3′UTR of SOCS3. The inhibition of SOCS3 could largely rescue the inhibitory effect of miR-30a-5p inhibition on CCA cells proliferation. In clinical, up-regulated miR-30a-5p expression was correlated with large tumor size in both ICC and ECC cohorts. Conclusions: miR-30a-5p promoted CCA cells proliferation through targeting SOCS3. These findings suggested that miR-30a-5p could be a potential therapeutic target.

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Single-Cell Transcriptome Reveals Cell Type–Specific Molecular Pathology in a 2VO Cerebral Ischemic Mouse Model

Zhang,

Xu,

Guo

et al. 2024

Mol Neurobiol

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Post-ischemia memory impairment is a major sequela in cerebral ischemia patients. However, cell type–specific molecular pathology in the hippocampus after ischemia is poorly understood. In this study, we adopted a mouse two-vessel occlusion ischemia model (2VO model) to mimic cerebral ischemia–induced memory impairment and investigated the single-cell transcriptome in the hippocampi in 2VO mice. A total of 27,069 cells were corresponding 14 cell types with neuronal, glial, and vascular lineages. We next analyzed cell-specific gene alterations in 2VO mice and the function of these cell-specific genes. Differential expression analysis identified cell type–specific genes with altered expression in neurons, astrocytes, microglia, and oligodendrocytes in 2VO mice. Notably, four subtypes of oligodendrocyte precursor cells with distinct differentiation pathways were suggested. Taken together, this is the first single-cell transcriptome analysis of gene expression in a 2VO model. Furthermore, we suggested new types of oligodendrocyte precursor cells with angiogenesis and neuroprotective potential, which might offer opportunities to identify new avenues of research and novel targets for ischemia treatment.

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MiR-30a-5p frequently downregulated in prostate cancer inhibits cell proliferation via targeting PCLAF

Cited by 31 publications

References 41 publications

miR‐30a inhibits androgen‐independent growth of prostate cancer via targeting MYBL2, FOXD1, and SOX4

miR‐30a inhibits androgen‐independent growth of prostate cancer via targeting MYBL2, FOXD1, and SOX4

MiR-30a-5p promotes cholangiocarcinoma cell proliferation through targeting SOCS3

Single-Cell Transcriptome Reveals Cell Type–Specific Molecular Pathology in a 2VO Cerebral Ischemic Mouse Model

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