MicroRNA‑665 suppresses the growth and migration of ovarian cancer cells by targeting HOXA10

Liu, Jinhui; Jiang, Yi; Wan, Yicong; Zhou, Shulin; Thapa, Sunita; Cheng, Wenjun

doi:10.3892/mmr.2018.9252

Cited by 28 publications

(33 citation statements)

References 38 publications

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“…Western blot analysis was conducted to examine the expression levels of p-β-catenin, β-catenin, and cyclin D1. ovarian cancer 29 and pancreatic cancer. 36 However, the expression profile of miR-665 in RB had not been investigated previously.…”

Section: Discussionmentioning

confidence: 99%

“…27 In contrast, miR-665 plays an inhibitory role in the growth and invasion of ovarian cancer cells. 29 A study by Dong et al revealed that upregulation of miR-665 expression attenuated the proliferation, invasion, and epithelial-mesenchymal transition of osteosarcoma cells. 28 However, the functional roles of miR-665 in RB cells have remained largely unknown.…”

Section: Discussionmentioning

confidence: 99%

“…Abnormal miR-665 expression has been reported in multiple human cancers. [26][27][28][29] However, the expression profile and biological function of miR-665 in RB and the underlying molecular mechanisms are largely unknown. Hence, in this study, we aimed to detect miR-665 expression in RB and evaluate its clinical value in patients with RB.…”

Section: Introductionmentioning

confidence: 99%

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<p>MicroRNA-665 inhibits the oncogenicity of retinoblastoma by directly targeting high-mobility group box 1 and inactivating the Wnt/β-catenin pathway</p>

Wang

et al. 2019

CMAR

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Purpose: Previous studies have revealed that microRNA-665 (miR-665) is dysregulated in a variety of human cancers. However, little is known regarding its expression profiles and functions in retinoblastoma (RB). Therefore, the aims of our study were to evaluate miR-665 expression in RB and determine the precise roles of miR-665 in the progression of RB. Patients and methods: Herein, RT-qPCR was used to determine miR-665 expression levels in RB tissues and cell lines, and a series of functional experiments were performed to explore the influence of miR-665 on RB cell proliferation, colony formation, apoptosis, migration, and invasion as well as tumor growth. The molecular mechanisms underlying the tumor-suppressive action of miR-665 in RB were also explored. Results: We found that miR-665 was markedly reduced in RB tissues and cell lines and that lower miR-665 expression was strongly associated with tumor size, TNM stage, and differentiation in patients with RB. Exogenous expression of miR-665 suppressed cell proliferation, colony formation, migration, and invasion, and induced cell apoptosis in RB cells, while silencing miR-665 expression had the opposite effects. In addition, upregulation of miR-665 decreased the tumor growth of RB cells in vivo. High-mobility group box 1 (HMGB1) was identified as a direct target of miR-665 in RB cells, and decreasing the expression of HMGB1 simulated the regulatory effects of miR-665 overexpression in RB cells, while knockdown of HMGB1 expression counteracted the miR-665-mediated antitumor effects in RB cells. Moreover, miR-665 was shown to regulate the Wnt/β-catenin signaling pathway by targeting HMGB1 in vitro and in vivo. Conclusion: Taken together, our in vitro and in vivo results suggest that miR-665 acts as a tumor-suppressive miRNA in RB by directly targeting HMGB1 and inactivating the Wnt/βcatenin pathway. Hence, this miRNA is a candidate prognostic biomarker and therapeutic target in patients with RB.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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<p>MicroRNA-665 inhibits the oncogenicity of retinoblastoma by directly targeting high-mobility group box 1 and inactivating the Wnt/β-catenin pathway</p>

Wang

et al. 2019

CMAR

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“…In breast cancer, tumor cell migration and invasion are enhanced by the overexpression of miR-665 by promoting the epithelial-mesenchymal transition process (34). By contrast, miR-665 has been demonstrated to suppress cell proliferation and migration in ovarian cancer cells (35). This controversy on the role of miR-665 may be due to the different cancer types.…”

Section: Discussionmentioning

confidence: 99%

Upregulated miR‑665 expression independently predicts poor prognosis of lung cancer and facilitates tumor cell proliferation, migration and invasion

Xia

Zhu

et al. 2020

Oncol Lett

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Non-small cell lung cancer (NSCLC) is one of the leading causes of global cancer-associated mortality. Aberrant microRNAs (miRs) have been reported to be involved in the pathogenesis of various cancer types. The present study aimed to investigate the expression profile and prognostic value of miR-665 in patients with NSCLC, and to analyze its functional role in tumor progression using NSCLC cells. Reverse transcription-quantitative PCR was used to estimate the expression levels of miR-665. Kaplan-Meier survival curves and Cox regression analysis were performed to evaluate the prognostic value of miR-665. The effects of miR-665 on NSCLC cell proliferation, migration and invasion were examined by cell transfection, and the target gene of miR-665 was explored. miR-665 expression was elevated in the tissue and cell samples of NSCLC. This increased miR-665 expression was associated with lymph node metastasis and TNM stage. An independent association between miR-665 and overall survival was identified in patients with NSCLC. When regulating the expression levels of miR-665 in vitro, NSCLC cell proliferation, migration and invasion were enhanced by overexpression of miR-665, but were inhibited by knockdown of miR-665. The luciferase activity results indicated that the protein tyrosine phosphatase receptor type B (PTPRB) was a direct target of miR-665 in NSCLC cells. The present study provided evidence for the clinical significance of a decreased expression of miR-665 in the prognosis of NSCLC. Upregulation of miR-665 contributed to tumor cell proliferation, migration and invasion by targeting PTPRB, suggesting the potential of miR-665 as a candidate therapeutic target for NSCLC treatment.

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“…MicroRNA‐665 was downregulated in ovarian cancer, pancreatic cancer, hepatocellular carcinoma, inflammatory bowel disease, and so on. However, the role and mechanism of miR‐665 in CC remains unknown.…”

Section: Discussionmentioning

confidence: 99%

DANCR‐mediated microRNA‐665 regulates proliferation and metastasis of cervical cancer through the ERK/SMAD pathway

et al. 2019

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Emerging evidence has indicated that microRNAs (miRNAs) play an important role in cervical cancer (CC). However, the role of miRNA (miR)‐665 in cervical cancer remains unclear. The aim of the present study was to investigate the potential functions of miR‐665 in CC and to identify the underlying mechanisms of action. Herein, we show that miR‐665 was downregulated in CC tissues and cell lines, which is negatively correlated with tumor size, distant metastasis, advanced TNM stage and poor prognosis. Functionally, miR‐665 inhibited cell proliferation, migration and invasion and resistance of cisplatin for CC cells, as well as tumor growth. We validated that transforming growth factor beta receptor 1 (TGFBR1) was a direct target of miR‐665 and mediated the ERK/SMAD pathway. In addition, we identified miR‐665 as the competing endogenous RNA for long noncoding (lnc)‐DANCR. These observations suggested that lnc‐DANCR‐mediated miR‐665 downregulation regulates the malignant phenotype of CC cells by targeting TGFBR1 through the ERK/SMAD pathway, which may present a pathway for novel therapeutic stratagems for CC therapy.

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MicroRNA‑665 suppresses the growth and migration of ovarian cancer cells by targeting HOXA10

Cited by 28 publications

References 38 publications

<p>MicroRNA-665 inhibits the oncogenicity of retinoblastoma by directly targeting high-mobility group box 1 and inactivating the Wnt/β-catenin pathway</p>

<p>MicroRNA-665 inhibits the oncogenicity of retinoblastoma by directly targeting high-mobility group box 1 and inactivating the Wnt/β-catenin pathway</p>

Upregulated miR‑665 expression independently predicts poor prognosis of lung cancer and facilitates tumor cell proliferation, migration and invasion

DANCR‐mediated microRNA‐665 regulates proliferation and metastasis of cervical cancer through the ERK/SMAD pathway

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MicroRNA‑665 suppresses the growth and migration of ovarian cancer cells by targeting HOXA10

Cited by 28 publications

References 38 publications

<p>MicroRNA-665 inhibits the oncogenicity of retinoblastoma by directly targeting high-mobility group box 1 and inactivating the Wnt/&beta;-catenin pathway</p>

<p>MicroRNA-665 inhibits the oncogenicity of retinoblastoma by directly targeting high-mobility group box 1 and inactivating the Wnt/&beta;-catenin pathway</p>

Upregulated miR‑665 expression independently predicts poor prognosis of lung cancer and facilitates tumor cell proliferation, migration and invasion

DANCR‐mediated microRNA‐665 regulates proliferation and metastasis of cervical cancer through the ERK/SMAD pathway

Contact Info

Product

Resources

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<p>MicroRNA-665 inhibits the oncogenicity of retinoblastoma by directly targeting high-mobility group box 1 and inactivating the Wnt/β-catenin pathway</p>

<p>MicroRNA-665 inhibits the oncogenicity of retinoblastoma by directly targeting high-mobility group box 1 and inactivating the Wnt/β-catenin pathway</p>