<i>miR-4429</i>Inhibits Tumor Progression and Epithelial-Mesenchymal Transition Via Targeting<i>CDK6</i>in Clear Cell Renal Cell Carcinoma

Pan, Hong; Hong, Yejing; Yu, Biying; Li, Li; Zhang, Xiaojian

doi:10.1089/cbr.2018.2697

Cited by 25 publications

(21 citation statements)

References 26 publications

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“…It was found that miR-4429 targeted DLEU1 in GBM cells. MiR-4429 was demonstrated in previous work to act as an anti-tumor miRNA, such as clear cell renal cell carcinoma [46] and papillary thyroid cancer [47]. Our study uncovered that inhibition of miR-4429 aggravated GBM cell growth, consolidating its tumor-suppressive role in GBM.…”

Section: Discussionsupporting

confidence: 53%

SP1–DLEU1–miR-4429 feedback loop promotes cell proliferative and anti-apoptotic abilities in human glioblastoma

Chen

Liu

2019

Bioscience Reports

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Mounting studies have revealed that long non-coding RNA (lncRNA) deleted in lymphocytic leukemia 1 (DLEU1) positively regulated the initiation and development of various human malignant tumors. Nevertheless, the function and mechanism of DLEU1 in human glioblastoma multiforme (GBM) remain elusive and ill-defined. The current study was designed to highlight the functional role and disclose the underlying molecular mechanism by which DLEU1 regulated GBM development. We found that DLEU1 was up-regulated in GBM and DLEU1 knockdown significantly inhibited GBM cell proliferation and induced apoptosis. As predicted by bioinformatics analysis and validated in mechanistic assays, SP1 could bind to the promoter region of DLEU1 to activate DLEU1 transcription. Additionally, miR-4429 was verified as a target gene of DLEU1 and negatively modulated by DLEU1. More importantly, miR-4429 overexpression repressed the mRNA and protein levels of SP1 via binding to the 3′UTR of SP1. Overexpression of SP1 or miR-4429 inhibitor could partly abolish the effect of DLEU1 knockdown on cell viability and apoptosis in GBM. Accordingly, our experimental data revealed that SP1–DLEU1–miR-4429 formed a feedback loop to promote GBM development, providing a new evidence for the role of DLEU1 in GBM.

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Section: Discussionsupporting

confidence: 53%

SP1–DLEU1–miR-4429 feedback loop promotes cell proliferative and anti-apoptotic abilities in human glioblastoma

Chen

Liu

2019

Bioscience Reports

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“…MiR-4429 promotes cervical cancer cell radio-sensitivity through RAD51 [26]. MiR-4429 suppresses cell proliferation, migration, invasion, and EMT via modulating CDK6 in clear cell renal cell carcinoma [27]. Furthermore, miR-4429 was proved to be sponged and negatively regulated by NR2F2-AS1 in cervical cancer.…”

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confidence: 97%

NR2F2-AS1 accelerates cell proliferation through regulating miR-4429/MBD1 axis in cervical cancer

et al. 2020

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Cervical cancer is one of the most frequent malignant tumors in female. Increasing studies have demonstrated that long noncoding RNAs (lncRNAs) play a key role in the development of multiple cancers. Although some studies have confirmed that lncRNA NR2F2 antisense RNA 1 (NR2F2-AS1) is a pro-cancer gene in many cancers, the molecular mechanism of NR2F2-AS1 in cervical cancer has not been completely elucidated. In the present study, our results revealed that NR2F2-AS1 expression was up-regulated in cervical cancer tissues and cells, notably in patients with advanced cervical cancer. NR2F2-AS1 accelerated progression of cervical cancer by facilitating cell proliferation, migration, invasion, and EMT process, but inhibiting cell apoptosis. Moreover, NR2F2-AS1 acted as a molecular sponge of miR-4429 and methyl-CpG-binding domain protein 1 (MBD1) was a downstream target of miR-4429 in cervical cancer. Furthermore, there was a negative correlation between miR-4429 expression and NR2F2-AS1 or MBD1 expression in tumor tissues. Rescue experiments confirmed that MBD1 overexpression partly rescued NR2F2-AS1 knockdown-mediated inhibition of progression in cervical cancer. To sum up, these results suggested the potential mechanism of NR2F2-AS1 in cervical cancer and revealed that NR2F2-AS1 exerted its carcinogenic effect via regulating miR-4429/MBD1 axis, indicating a promising insight into the therapeutic target of cervical cancer.

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“…miR‐4429 has been reported to be downregulated and functioned as a tumor‐suppressor gene in papillary thyroid cancer (W. J. Wu et al, ). Furthermore, the antioncogenic role of miR‐4429 has been verified in clear cell renal cell carcinoma via targeting CDK6 (Pan, Hong, Yu, Li, & Zhang, ). In concordance, present study first identified that miR‐4429 was downregulated in CC cell lines compared with normal cell line.…”

Section: Discussionmentioning

confidence: 99%

miR‐4429 sensitized cervical cancer cells to irradiation by targeting RAD51

Sun

Fan

Deng

et al. 2019

Journal Cellular Physiology

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Cervical cancer (CC) is a prevalent malignancy in women, with the feature of metastasis and easy recurrence is responsible for a large proportion of global cancer deaths. Radiotherapy is one of the common treatment tools for CC patients with unresectable tumors. However, radio-resistance in patients could be a major reason for recurrence. Therefore, it is of significance to tunnel the molecular mechanism of radio-resistance in CC. MicroRNAs (miRNAs) are increasingly reported in the regulation of cancer progression and cellular response to radiotherapy and chemotherapy. miR-4429 is a newly discovered miRNA acting as a tumor-suppressor gene in multiple cancers, but its function in CC has never been explored yet. The current study tried to explore the role of miR-4429 in cell radio-sensitivity in CC.First, we validated the downregulation of miR-4429 in CC cells. Importantly, the association of miR-4429 with radio-resistance was validated by identifying the downregulation of miR-4429 in radio-resistant CC cells. Gain-and loss-of-function assays validated that miR-4429 sensitized CC cells to irradiation. Through bioinformatics tools, RAD51 recombinase (RAD51) was identified to be a target for miR-4429. RAD51 is known to be a crucial regulator for DNA damage repair and has been reported to influence cell radio-resistance in cancers, including in CC. Luciferase reporter assay confirmed the interaction between miR-4429 and RAD51. Finally, rescue assays indicated that miR-4429 promoted CC cell radio-sensitivity through RAD51. Consequently, our study showed that miR-4429 sensitized CC cells to irradiation by targeting RAD51, providing a potential therapeutic target for CC patients. K E Y W O R D Scervical cancer, miR-4429, RAD51, radio-resistance

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miR-4429Inhibits Tumor Progression and Epithelial-Mesenchymal Transition Via TargetingCDK6in Clear Cell Renal Cell Carcinoma

Cited by 25 publications

References 26 publications

SP1–DLEU1–miR-4429 feedback loop promotes cell proliferative and anti-apoptotic abilities in human glioblastoma

SP1–DLEU1–miR-4429 feedback loop promotes cell proliferative and anti-apoptotic abilities in human glioblastoma

NR2F2-AS1 accelerates cell proliferation through regulating miR-4429/MBD1 axis in cervical cancer

miR‐4429 sensitized cervical cancer cells to irradiation by targeting RAD51

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