MiR‐646 suppresses proliferation and metastasis of non‐small cell lung cancer by repressing FGF2 and CCND2

Wang, Jing; Shu, Huizhen; Guo, Sisi

doi:10.1002/cam4.3062

Cited by 32 publications

(28 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“… 16 Wang et al found that FGF2 is a target gene of miR-646 in NSCLC and that miR-646 might reduce the proliferation and invasion ability of NSCLC by inhibiting FGF2. 17 In the present study, the FGF2 expression significantly reduced in the A549/DDP cells with overexpression of miR-195-5p upon WB assay and PCR, while the FGF2 expression significantly elevated in the A549 cells with inhibited expression of miR-195-5p. Via the dual-luciferase reporter assay, FGF2 was confirmed to be the direct target gene of miR-195-5p, which could improve the chemosensitivity of cisplatin-resistant LC cells through FGF2 and inhibit migration and invasion.…”

Section: Discussionsupporting

confidence: 48%

Reversal of Chemotherapy Resistance to Cisplatin in NSCLC by miRNA-195-5p via Targeting the FGF2 Gene

Wang¹,

Sui²,

Wu³

et al. 2021

PGPM

View full text Add to dashboard Cite

Objective To explore the mechanism of miR-195-5p in the pathogenesis non-small cell lung cancer (NSCLC) and cisplatin resistance. Methods The function of miR-195-5p in NSCLC and cisplatin resistance were determined by MTT, scratch assay, transwell assay, and nude mice xenograft experiments. miR-195-5p target gene was identified by dual-luciferase reporter assays and real-time PCR analysis. Results miR-195-5p content was lower in A549/DDP than that in A549 cells, with reduced chemotherapy sensitivity and increased cell invasion and migration ability. The loss-of-function and gain-of-function assays illustrated that miR-195-5p might have increased the chemosensitivity to cisplatin in the A549/DDP cells and decreased cell migration and invasion. FGF2 is a negatively correlated action target of miR-195-5p. miR-195-5p might affect EMT by inhibiting FGF2. Overexpression of FGF2 resulted in enhanced cisplatin resistance in the cells, while miR-195-5p might have reversed this resistance. Conclusion Overall, miR-195-5p might target FGF2 to reduce cisplatin resistance in A549/DDP cells and enhance chemosensitivity.

show abstract

Section: Discussionsupporting

confidence: 48%

Reversal of Chemotherapy Resistance to Cisplatin in NSCLC by miRNA-195-5p via Targeting the FGF2 Gene

Wang¹,

Sui²,

Wu³

et al. 2021

PGPM

View full text Add to dashboard Cite

show abstract

“…MiR-646 suppresses clear cell renal carcinoma cell metastasis by downregulating nin one binding protein [29]. MiR-646 is involved in inhibiting proliferation and metastasis of non-small cell lung cancer by binding to FGF2 and CCND2 [30]. These studies suggested that miR-646 plays an anticancer role in a variety of tumors.…”

Section: Discussionmentioning

confidence: 95%

Circ_0000527 promotes the progression of retinoblastoma by regulating miR-646/LRP6 axis

Zhang¹,

Wu²,

Li³

et al. 2020

Cancer Cell Int

View full text Add to dashboard Cite

Background: Researches validate that circular RNAs (circRNAs) are dysregulated in a variety of malignancies and play an important role in regulating the malignant phenotype of tumor cells. Nevertheless, the role of circ_0000527 in retinoblastoma (RB) and its regulatory mechanisms remain largely unknown. Methods: Real-time PCR (RT-PCR) was used to detect circ_0000527 and miR-646 expression in RB tissues and cells. The LRP6 expression in RB cells was detected by Western blot. The relationship between circ_0000527 expression and the clinicopathological parameters of RB patients was analyzed. Cell proliferation, apoptosis and metastasis were monitored by cell counting kit-8 (CCK-8), flow cytometry, and Transwell assay. The dual-luciferase reporter gene assay and RIP assay were employed to verify the targeting relationship between circ_0000527 and miR-646, miR-646 and LRP6. Results: Circ_0000527 was highly expressed in both RB and RB cell lines, whose high expression level and degree of differentiation were significantly correlated with the increase in cTNM staging level. Overexpression of circ_0000527 contributed to RB cell proliferation, migration, invasion and suppressed cell apoptosis, while knocking down circ_0000527 inhibited the above malignant biological behavior. The underlying mechanism suggested that functioning as a endogenous competitive RNA, circ_0000527 directly targeted miR-646 and positively regulated LRP6 expression. Conclusion: Circ_0000527 enhances the proliferation and metastasis of RB cells by modulating the miR-646/LRP6 axis.

show abstract

“…In addition, miR-646 and miR-381-3p are derived from human chromosomes 20 and 14, respectively, and their roles in tumours have been extensively reported. miR-646 has been indicated to function as a tumour suppressor in retinoblastoma (29), endometrial carcinoma (30), non-small-cell lung cancer (31), laryngeal squamous cell carcinoma (32), and CRC (33). miR-381-3p also functions as a tumour suppressor in non-small-cell lung cancer (34), oral squamous cell carcinoma (35), breast cancer (36), and cervical cancer (37).…”

Section: Discussionmentioning

confidence: 99%

The LncRNA CASC11 Promotes Colorectal Cancer Cell Proliferation and Migration by Adsorbing miR-646 and miR-381-3p to Upregulate Their Target RAB11FIP2

Zhang

et al. 2021

Front. Oncol.

View full text Add to dashboard Cite

BackgroundWe previously reported that the long non-coding RNA (lncRNA) CASC11 promotes colorectal cancer (CRC) progression as an oncogene by binding to HNRNPK. However, it remains unknown whether CASC11 can act as a competitive endogenous RNA (ceRNA) in CRC. In this study, we focused on the role of CASC11 as a ceRNA in CRC by regulating miR-646 and miR-381-3p targeting of RAB11FIP2.MethodsWe identified the target microRNAs (miRNAs) of CASC11 and the target genes of miR-646 and miR-381-3p using bioinformatic methods. A dual-luciferase reporter assay was performed to validate the target relationship. Quantitative real-time PCR (qRT-PCR), western blotting (WB), and immunohistochemistry (IHC) were used to measure the RNA and protein expression levels. Rescue experiments in vitro and in vivo were performed to investigate the influence of the CASC11/miR-646 and miR-381-3p/RAB11FIP2 axis on CRC progression.ResultsWe found that CASC11 binds to miR-646 and miR-381-3p in the cytoplasm of CRC cells. Moreover, miR-646 and miR-381-3p inhibitors reversed the suppressive effect of CASC11 silencing on CRC growth and metastasis in vitro and in vivo. We further confirmed that RAB11FIP2 is a mutual target of miR-646 and miR-381-3p. The expression levels of CASC11 and RAB11FIP2 in CRC were positively correlated and reciprocally regulated. Further study showed that CASC11 played an important role in regulating PI3K/AKT pathway by miR-646 and miR-381-3p/RAB11FIP2 axis.ConclusionOur study showed that CASC11 promotes the progression of CRC as a ceRNA by sponging miR-646 and miR-381-3p. Thus, CASC11 is a potential biomarker and a therapeutic target of CRC.

show abstract

MiR‐646 suppresses proliferation and metastasis of non‐small cell lung cancer by repressing FGF2 and CCND2

Cited by 32 publications

References 21 publications

Reversal of Chemotherapy Resistance to Cisplatin in NSCLC by miRNA-195-5p via Targeting the FGF2 Gene

Reversal of Chemotherapy Resistance to Cisplatin in NSCLC by miRNA-195-5p via Targeting the FGF2 Gene

Circ_0000527 promotes the progression of retinoblastoma by regulating miR-646/LRP6 axis

The LncRNA CASC11 Promotes Colorectal Cancer Cell Proliferation and Migration by Adsorbing miR-646 and miR-381-3p to Upregulate Their Target RAB11FIP2

Contact Info

Product

Resources

About