Downregulation of miR-4443 and miR-5195-3p in ovarian cancer tissue contributes to metastasis and tumorigenesis

Ebrahimi, Seyed Omar; Reiisi, Somayeh

doi:10.1007/s00404-019-05107-x

Cited by 40 publications

(30 citation statements)

References 21 publications

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“…The in vitro experiments demonstrated that miR-5195-3p overexpression reduced proliferation and induced a G0/G1 cell cycle block in PCa cells (PC-3 and DU145). Consistent with our in vitro data, signi cant reduction in miR-5195-3p was observed in cancer samples and its reduction was correlated with increased cell proliferation in ovarian cancer [23]. Jiang et al [17] showed that miR-5195-3p suppressed proliferation and invasion of human bladder cancer cells.…”

Section: Discussionsupporting

confidence: 89%

MiR-5195-3p Functions as a Tumor Suppressor in Prostate Cancer via Targeting CCNL1

Zeng

Shen

et al. 2020

Preprint

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BackgroundAccumulating evidence indicates miR-5195-3p exerts tumor suppressive role in several tumors. However, there is limited research on the clinical significance and biological function of miR-5195-3p in prostate cancer (PCa).MethodsExpression levels of miR-5195-3p and Cyclin L1 (CCNL1) were determined using quantitative real-time PCR. The clinical significance of miR-5195-3p in PCa patients was evaluated using Kaplan-Meier survival analysis and Cox regression models. Cell proliferation and cell cycle distribution were measured by CCK-8 assay and flow cytometry, respectively. The association between miR-5195-3p and CCNL1 was analyzed by luciferase reporter assay.ResultsMiR-5195-3p expression levels were significantly downregulated in 69 paired PCa tissues compared with matched adjacent normal tissues. The decreased miR-5195-3p expression was associated with Gleason score and TNM stage, as well as worse survival prognosis. The in vitro experiments showed that miR-5195-3p overexpression suppressed the proliferation and cell cycle G1/S transition in PC-3 and DU145 cells. Elevated miR-5195-3p abundance was also demonstrated to impair tumor formation in vivo using PC-3 xenografts. Mechanistically, Cyclin L1 (CCNL1) was a direct target of miR-5195-3p in PCa cells, which was inversely correlated with miR-5195-3p in PCa tissues. Importantly, CCNL1 knockdown imitated, while overexpression reversed the effects of miR-5195-3p overexpression on PCa cell proliferation and cell cycle G1/S transition.ConclusionsOur data suggests that miR-5195-3p functions as a tumor suppressor via downregulating G1/S related CCNL1 expression in PCa.

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Section: Discussionsupporting

confidence: 89%

MiR-5195-3p Functions as a Tumor Suppressor in Prostate Cancer via Targeting CCNL1

Zeng

Shen

et al. 2020

Preprint

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“…Another study showed that miR‐4443 promoted Epi resistance in non‐small‐cell lung cancer by downregulating inositol polyphosphate‐4‐phosphatase Type I A and activating Janus kinase 2/signal transducer and activator of transcription 3 pathway (W. Zhang et al, 2018). However, miR‐4443 showed a beneficial effect in ovarian cancer, glioblastoma, osteosarcoma, hepatocellular carcinoma, and colon cancer (Ebrahimi & Reiisi, 2019; Gao et al, 2019; Gong, Wang, Liu, Hu, & Zheng, 2018; Meerson & Yehuda, 2016; C. Zhou et al, 2018). Taking together, miR‐4443 may play different roles in different cancers.…”

Section: Discussionmentioning

confidence: 99%

Microenvironment‐induced TIMP2 loss by cancer‐secreted exosomal miR‐4443 promotes liver metastasis of breast cancer

Wang

Zhang

Wang

et al. 2020

Journal Cellular Physiology

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We aimed to investigate the role of exosomal miR‐4443 in metastasis of breast cancer (BCa). In vitro wound‐healing assay and transwell invasion assay were used to investigate effect of miR‐4443 on BCa cells. Animal experiments were performed to confirm its effects in vivo. miR‐4443 promotes the metastasis of BCa cells through downregulating tissue inhibitors of metalloproteinase 2 (TIMP2) and upregulating matrix metalloproteinases (MMPs). Highly invasive BCa cells have a higher expression of miR‐4443 in both cells and exosomes. The exosomes derived from highly invasive BCa cells mainly gather in the primary tumor and liver. In vivo, overexpression of miR‐4443 in noninvasive BCa cells induces liver metastasis, accompanied with downregulated TIMP2, and upregulated MMP‐2 in both the primary tumor and liver. When we armed MCF‐10A exosomes with miR‐4443 inhibitors to treat mice bearing high‐miR‐4443 tumors, exosomes accumulated in the primary tumor, and liver following the upregulation of TIMP2 and downregulation of MMP2, and the metastasis was inhibited. Highly invasive BCa cells destroy natural barriers against metastasis by delivering exosomal miR‐4443 to stromal cells of the primary tumor and impairing TIMP2, consequently activating MMP; circulating exosomal miR‐4443 might promote BCa cells lodging in future metastatic sites through the similar mechanisms.

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“…Some studies report that lncRNAs can function as competitive endogenous RNAs (ceRNAs) or miRNA sponges to achieve their functions 18 . Hsa-miR-4443 is involved in a variety of tumors 19 , 20 , and many studies have confirmed the relationship between lncRNA and miR-4443. It is suggested that lncRNA FEZF1-AS1 could contribute to hepatocellular carcinoma progression by regulating miR-4443 21 .…”

Section: Introductionmentioning

confidence: 97%

Long Noncoding RNA LINC00460 Promotes Cell Progression by Sponging miR-4443 in Head and Neck Squamous Cell Carcinoma

Zhang

Ding

et al. 2020

Cell Transplant

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Head and neck squamous cell carcinoma (HNSCC) is one of the most common cancers worldwide. Long noncoding RNAs were proved to be associated with the development and progression in HNSCC. However, the mechanism of LINC00460 in HNSCC needs to be further investigated. The study used quantitative real-time polymerase chain reaction assay to detect the expression of LINC00460 in cancer tissues and cell lines. Gain and loss of function experiments were conducted to analyze the effects of LINC00460 and miR-4443 on cell proliferation, invasion, and apoptosis of HNSCC cells in vitro. The interactions among miR-4443 and LINC00460 were detected by dual-luciferase reporter assay. Here, the study showed that LINC00460 was highly expressed in HNSCC tissues and cell lines. Functionally, knockdown of LINC00460 inhibited HNSCC cell proliferation and migration in vitro. Besides, LINC00460 promoted cell progression by sponging miR-4443, and miR-4443 inhibitor could reverse the effects of si-LINC00460 on cell proliferation and migration. In summary, LINC00460 could potentially promote cell progression and epithelial mesenchymal transition by sponging miR-4443 in HNSCC. LINC00460 could be used as a potential therapeutic target for HNSCCs.

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Downregulation of miR-4443 and miR-5195-3p in ovarian cancer tissue contributes to metastasis and tumorigenesis

Cited by 40 publications

References 21 publications

MiR-5195-3p Functions as a Tumor Suppressor in Prostate Cancer via Targeting CCNL1

MiR-5195-3p Functions as a Tumor Suppressor in Prostate Cancer via Targeting CCNL1

Microenvironment‐induced TIMP2 loss by cancer‐secreted exosomal miR‐4443 promotes liver metastasis of breast cancer

Long Noncoding RNA LINC00460 Promotes Cell Progression by Sponging miR-4443 in Head and Neck Squamous Cell Carcinoma

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