MicroRNA‑665 promotes the proliferation of ovarian cancer cells by targeting SRCIN1

Zhou, Ping; Xiong, Tingchuan; Yao, Lili; Yuan, Jianlin

doi:10.3892/etm.2019.8293

Cited by 15 publications

(17 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In ovarian cancer, sustained activation of MAPK/ERK signaling is associated with strong cell proliferation and metastatic potential (73). The western blotting results showed that inhibition of miR-665 increased SRCIN1, at both the mRNA and protein level, and inactivated MAPK/ERK pathway in ovarian cancer (74). Similar findings were reported in the case of miR-150.…”

Section: Mirna-mediated Src Oncogenic Signaling In Selected Cancer Typessupporting

confidence: 72%

Historical retrospective of the SRC oncogene and new perspectives (Review)

et al. 2020

View full text Add to dashboard Cite

Since its first discovery as part of the Rous sarcoma virus (RSV) genome, the c-SRC (SRC) proto-oncogene has been proved a key regulator of cancer development and progression, and thus it has been highlighted as an attractive target for anti-cancer therapeutic strategies. Though the exact mechanisms of its action are still not fully understood, SRC protein mediates crucial normal cell functions, such as cell development, proliferation and survival, and its dysregulation is considered as an oncogenic signature and a driving force for cancer initiation. In the present review, we present a flashback to the history of the Src research, while focusing on the most important milestones in the field. Moreover, we investigate the proposed regulatory mechanisms and molecules that mediate its action in order to designate putative therapeutic targets and useful prognostic and/or diagnostic tools. Furthermore, we present and discuss existing therapeutic approaches that are explored in clinical settings. Contents 1. Introduction 2. Discovery of Rous sarcoma virus 3. Cellular origin of retroviral oncogenes 4. MicroRNAs as the fine tuners of SRC oncogenic signaling 5. miRNA-mediated SRC oncogenic signaling in selected cancer types 6. Exosomes as the fine tuners of oncogenic signaling 7. SRC inhibitors as anticancer agents in clinical trials 8. Conclusion

show abstract

Section: Mirna-mediated Src Oncogenic Signaling In Selected Cancer Typessupporting

confidence: 72%

Historical retrospective of the SRC oncogene and new perspectives (Review)

et al. 2020

View full text Add to dashboard Cite

show abstract

“…A plethora of studies have found that miRNAs are involved in multiple steps of tumor diseases, including growth, migration, invasion, metabolism and metastasis [ 25 , 26 ]. Currently, only a few studies have found that miR-665 play an important role in some cancers [ 18 , 21 ]. A previous study reveals that miR-665 expression is correlated with breast cancer survival and miR-665 expression predicts poor and promotes tumor metastasis by targeting NR4A3 [ 19 ].…”

Section: Discussionmentioning

confidence: 99%

“…Some studies have found that miRNAs are involved in the oncogenesis, development and transformation of LUSC, such as miR-182-5p, miR-198-5p, miR-223-3p, miR-372-3p [ 14 – 17 ]. Previous studies have shown that miR-665 is clinically significant and regulates oncogenesis and development in breast cancer, ovarian cancer, liver cancer, gastric cancer, pancreatic cancer, retinoblastoma and lymphoblastic leukemia [ 18 – 21 ]. However, the clinical significance, precise molecular mechanisms and biological functions of miR-665 in LUSC remain unclear.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-665 facilitates cell proliferation and represses apoptosis through modulating Wnt5a/β-Catenin and Caspase-3 signaling pathways by targeting TRIM8 in LUSC

et al. 2021

View full text Add to dashboard Cite

Background MicroRNAs (miRNAs) are involved in the oncogenesis, development and transformation of lung squamous cell carcinoma (LUSC). miR-665 is clinically significant and acts as a pivotal function in some cancers. Nevertheless, the effects and the potential mechanisms of miR-665 in human LUSC are still unknown. Methods To analyse the clinical significant of miR-665 in human LUSC, quantitative real-time PCR (qRT-PCR) was use to measure miR-665 expression in LUSC specimen tissues and cell lines. Tripartite motif 8 (TRIM8) was verified a target of miR-665 by performing bioinformatic prediction and luciferase reporter assay. The expression levels of TRIM8 were examined through qRT-PCR and Western blotting in LUSC specimen tissues. CCK8 assay was fulfilled for analyzing the function in LUSC cell proliferation. Flow cytometry was used to detect cell and apoptosis. TRIM8 silencing and overexpression further verified the biological effects as those caused by miR-665. Results Here we reported that miR-665 expression was upregulated in LUSC specimen tissues and cell lines. High miR-665 levels were related to differentiation, tumor size and TNM stage. miR-665 mimics facilitated LUSC cell growth and cell cycle G1-S transition and repressed apoptosis. miR-665 inhibitor suppressed cell proliferation and G1-S transition and promoted apoptosis. miR-665 expression was negatively correlated with TRIM8 mRNA expression in LUSC. Luciferase reporter assay confirmed that TRIM8 was a direct target gene of miR-665. miR-665 mimics downregulated the TRIM8 levels, and miR-665 inhibitor upregulated the TRIM8 levels in LUSC cells. Particularly, silencing TRIM8 led to the similar effects of miR-665 mimics in LUSC cells. Overexpression of TRIM8 inhibited LUSC cell proliferation in vitro and in vivo. Furthermore, miR-665 promoted LUSC cell proliferation through facilitating the Wnt5a/β-catenin signaling pathway and restrained apoptosis via inhibiting Caspase-3 signaling pathway, whereas TRIM8 suppressed cell growth by repressing the Wnt5a/β-catenin signaling pathway and induced apoptosis through activating Caspase-3 signaling pathway. Conclusions The current study demonstrates that miR-665 facilitates LUSC cell proliferation and cell cycle transition by regulation of the Wnt5a/β-Catenin signaling pathway and represses cell apoptosis via modulation of Caspase-3 signaling pathway by directly targeting TRIM8. These findings suggest that miR-665 might be a potential new target for LUSC therapy.

show abstract

“…During our study of tumor inhibition by circ-000881, miR-665 greatly aroused our interest because of its potential binding site with circ-000881, which was revealed by bioinformatics analysis. Many studies have demonstrated miR-665 to be abnormally expressed in tumors such as ovarian cancer (26), gastric adenocarcinoma (27) and hepatocellular carcinoma (28). Liu et al also found that miR-665 expression was upregulated in small cell lung cancer tissues (29).…”

Section: Discussionmentioning

confidence: 99%

Circular RNA hsa-circ-000881 suppresses the progression of lung adenocarcinoma in vitro via a miR-665/PRICKLE2 axis

Huang¹,

Yue²,

Li³

et al. 2021

Ann Transl Med

View full text Add to dashboard Cite

Background: Circular RNA (circRNA) has become a new focus in the field of tumor biology research in recent years. Many circRNAs have been showed to play an important role in the progression of lung adenocarcinoma (LUAD). In this work, we studied the oncological role of hsa-circ-000881 in LUAD and attempted to explore the related mechanism. Methods:The relative expressions of hsa-circ-000881, miR-665, and PRICKLE2 were detected by RT-qPCR or western blot. Functional assays were conducted to analyze the role of hsa-circ-000881 in the proliferation, migration, and invasion of LUAD cells. A luciferase reporter assay was performed to verify whether hsa-circ-000881, miR-665, and PRICKLE2 interact with each other.Results: Circ-000881 was remarkably downregulated in LUAD. Overexpression of circ-000881 attenuated cell growth, migration, and invasion, whereas its knockdown enhanced the malignancy of LUAD cells. The results of luciferase reporter assay and bioinformatics analysis confirmed that circ-000881 served as a sponge for miR-665, and PRICKLE2 was a direct target of miR-665.Overexpression of miR-665 or silencing of PRICKLE2 abolished circ-000881-mediated inhibition of malignant tumor behavior in LUAD cells.Conclusions: Circ-000881 has inhibitory effects on LUAD via a miR-665/PRICKLE2 axis, suggesting that circ-000881 may be an underlying therapeutic target for LUAD.

show abstract

MicroRNA‑665 promotes the proliferation of ovarian cancer cells by targeting SRCIN1

Cited by 15 publications

References 34 publications

Historical retrospective of the SRC oncogene and new perspectives (Review)

Historical retrospective of the SRC oncogene and new perspectives (Review)

MicroRNA-665 facilitates cell proliferation and represses apoptosis through modulating Wnt5a/β-Catenin and Caspase-3 signaling pathways by targeting TRIM8 in LUSC

Circular RNA hsa-circ-000881 suppresses the progression of lung adenocarcinoma in vitro via a miR-665/PRICKLE2 axis

Contact Info

Product

Resources

About