Inhibition of miR-423-5p suppressed prostate cancer through targeting GRIM-19

Lin, Haili; Lin, Tianqi; Lin, Jiangui; Yang, Minggen; Shen, Zhiqing; Liu, Hongjie; Zou, Zong-kai; Zheng, Zhouda

doi:10.1016/j.gene.2018.11.021

Cited by 30 publications

(23 citation statements)

References 19 publications

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“…Furthermore, it was found that overexpression of LINC00968, low expression of hsa-miR-423-5p or upregulation of PROX1 results in the inhibition of proliferation, migration and angiogenesis of BC cells. Previous studies have provided evidence that the down-regulation of hsa-miR-423-5p is capable of inhibiting prostate cancer cell proliferation [33]. Another study established that miR-423-5p plays a functional role through its contribution in cell proliferation and invasion by targeting trefoil factor 1 in gastric cancer cells [34], suggesting that miR-423-5p acts as an oncogene in gastric cancer tissues and that it has therapeutic potential for gastric cancer.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Long non-coding RNA LINC00968 reduces cell proliferation and migration and angiogenesis in breast cancer through up-regulation of PROX1 by reducing hsa-miR-423-5p

et al. 2019

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Background: Breast cancer (BC) is a common invasive malignancy in women with unclear etiology. A recent study suggested that long non-coding RNA (lncRNA), LINC00968 had a tumor-promoting effect in cancer. However, the role of LINC00968 in BC remains unclear. Therefore, we conducted the present study to determine the effect of LINC00968 in BC and its underlying mechanism. Methods: The expression of LINC00968 and hsa-miR-423-5p in BC tissues and cells was determined using reverse transcription quantitative polymerase chain reaction and western blot analysis. Dual luciferase reporter, RNA pull-down and RNA immunoprecipitation assays were used to determine the relationship among LINC00968, PROX1 and hsa-miR-423-5p. Gain-and loss-function approaches were utilized to examine the effects of LINC00968, PROX1 and hsa-miR-423-5p on cell proliferation, migration, tube formation in vitro; and tumor growth and angiogenesis in vivo. Results: LINC00968 expression reduced while hsa-miR-423-5p increased in BC tissues relative to adjacent normal tissues. Overexpression of LINC00968 was observed to inhibit BC cell proliferation, migration and tube formation abilities in vitro as well as tumor growth in vivo through inhibition of hsa-miR-423-5p. And hsa-miR-423-5p mediated BC cellular functions and tumor growth through down-regulating PROX1. LINC00968 was identified as a competing endogenous RNA to upregulate PROX1 by downregulating hsa-miR-423-5p. More importantly, it was found that LINC00968 increased PROX1 expression in vivo in a concentration-dependent manner. Conclusion: Taken together, this study suggests that LINC00968 inhibits the progression of BC through impeding hsa-miR-423-5p-mediated PROX1 inhibition. LINC00968 may be a potential therapeutic target for BC therapy that warrants further studies.

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Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Long non-coding RNA LINC00968 reduces cell proliferation and migration and angiogenesis in breast cancer through up-regulation of PROX1 by reducing hsa-miR-423-5p

et al. 2019

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“…MiR-423-5p functioned as oncogene, contributing to malignant phenotypes and chemoresistance to temozolomide in glioblastomas ( 36 ). It was previously reported that the plasma level of miR-423-5p was a potential biomarker for diagnosis of colorectal cancer ( 37 ). However, the biological role of miR-423-5p in tumorigenesis and radiosensitivity in terms of CRC remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of miR-423-5p Contributes to the Radioresistance in Colorectal Cancer Cells

et al. 2021

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Resistance to radiotherapy is the main reason causing treatment failure in locally advanced rectal cancer. MicroRNAs (miRNAs) have been well demonstrated to regulate cancer development and progression. However, how miRNAs regulate radiotherapy resistance in colorectal cancer remains unknown. Herein, we established two human colorectal cancer cell lines resistant to radiotherapy, named HCT116-R and RKO-R, using the strategy of fractionated irradiation. The radioresistant phenotypical changes of the two cell lines were validated by cell viability assay, colony formation assay and apoptosis assay. The miRNA expression profilings of HCT116-R and RKO-R were determined using RNA-seq analyses, and further confirmed by quantitative real-time PCR. Multiple miRNAs, including miR-423-5p, miR-7-5p, miR-522-3p, miR-3184-3p, and miR-3529-3p, were identified with altered expression in both of the radiotherapy-resistant cells, compared to the parental cells. The downregulation of miR-423-5p was further validated in the rectal cancer tissues from radiotherapy-resistant patients. Silencing of miR-423-5p in parental HCT116 and RKO cells decreased the sensitivity to radiation treatment, and inhibited the radiation-induced apoptosis. In consistence, overexpression of miR-423-5p in HCT116-R and RKO-R cells partially rescued their sensitivity to radiotherapy, and promoted the radiation-induced apoptosis. Bcl-xL (Bcl-2-like protein 1) was predicted to be a potential target gene for miR-423-5p, and miR-423-5p/Bcl-xL axis could be a critical mediator of radiosensitivity in colorectal cancer cells. The current finding not only revealed a novel role of miR-423-5p in regulating the radiosensitivity in colorectal cancer, but also suggested miR-423-5p as a molecular candidate for combination therapy with radiation to treat colorectal cancer.

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“…Previously, miR-423-5p was demonstrated to act as a tumor suppressor or oncogene in the development of many types of cancer. For example, Lin and colleagues reported that inhibition of miR-423-5p can suppress the proliferation and promote the apoptosis of prostate cancer (25). Tang that miR-423-5p can act as a tumor suppressor gene in osteosarcoma through the regulation of STMN1 expression (27).…”

Section: Discussionmentioning

confidence: 99%

lncRNA FOXP4‑AS1 predicts poor prognosis and accelerates the progression of mantle cell lymphoma through the miR‑423‑5p/NACC1 pathway

et al. 2020

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Long non-coding RNA (lncRNA) forkhead box P4 antisense RNA 1 (FOXP4-AS1) has been determined to function as an oncogene in various types of cancer. However, the biological function and the underlying mechanisms of FOXP4-AS1 in mantle cell lymphoma (MCL) remain to be uncovered. The expression and the associated clinicopathological characteristics and prognostic significance of FOXP4-AS1 were explored in MCL clinical samples. The effects of FOXP4-AS1 on MCL cellular behaviors, including proliferation, migration and invasion were analyzed using CCK-8, crystal violet and Transwell assays. The downstream molecules of FOXP4-AS1 were explored using bioinformatics analysis and dual luciferase assay. Our results showed that FOXP4-AS1 expression was upregulated in MCL patients, and that the high expression of FOXP4-AS1 was correlated with the unfavorable prognosis of patients. Functionally, while FOXP4-AS1 downregulation inhibited proliferation, migration and invasion of MCL cells, FOXP4-AS1 overexpression had promotive effects on these cellular processes. Mechanistically, FOXP4-AS1 was found to act as a competing endogenous (ce)RNA for miR-423-5p to regulate the expression of nucleus accumbens-associated 1 (NACC1). The negative regulation of FOXP4-AS1 on miR-423-5p compared to that of miR-423-5p on NACC1 was determined at the mRNA or protein levels in MCL cells. Moreover, an inverse expression correlation between FOXP4-AS1 and miR-423-5p, and that between miR-423-5p and NACC1 was confirmed in MCL clinical samples. In addition, rescue assay showed that miR-423-5p upregulation or NACC1 knockdown abolished the promoting effects of FOXP4-AS1 on MCL cell proliferation, migration and invasion. In conclusion, FOXP4-AS1 promotes MCL progression through the upregulation of NACC1 expression by inhibiting miR-423-5p. FOXP4-AS1 may serve as a novel therapeutic target for patients with MCL.

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Inhibition of miR-423-5p suppressed prostate cancer through targeting GRIM-19

Cited by 30 publications

References 19 publications

RETRACTED ARTICLE: Long non-coding RNA LINC00968 reduces cell proliferation and migration and angiogenesis in breast cancer through up-regulation of PROX1 by reducing hsa-miR-423-5p

RETRACTED ARTICLE: Long non-coding RNA LINC00968 reduces cell proliferation and migration and angiogenesis in breast cancer through up-regulation of PROX1 by reducing hsa-miR-423-5p

Downregulation of miR-423-5p Contributes to the Radioresistance in Colorectal Cancer Cells

lncRNA FOXP4‑AS1 predicts poor prognosis and accelerates the progression of mantle cell lymphoma through the miR‑423‑5p/NACC1 pathway

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