miR-196b-5p–mediated downregulation of TSPAN12 and GATA6 promotes tumor progression in non-small cell lung cancer

Liang, Guang; Wang, Meng; Huang, Xiangjie; Zhu, Wenxiu; Yin, Changtian; Wang, Canwei; Fassan, Matteo; Yu, Yun; Kudo, M.; Xiao, Sisi; Zhao, Chengguang; Zou, Peng; Wang, Yumin; Li, Xiaokun; Croce, Carlo M.; Cui, Ri

doi:10.1073/pnas.1917531117

Cited by 128 publications

(96 citation statements)

References 40 publications

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“…MiRNAs are also ncRNA molecules with 18 ~ 25 nucleotides in length, and they play a biological role by targeting the downstream mRNAs [ 13 ]. As reported, miR-196b-5p promoted tumor development in NSCLC by targeting TSPAN12 and GATA6 [ 14 ]. MiR-212-5p enhanced tumor growth by regulating Id3 in lung adenocarcinoma cells [ 15 ].…”

Section: Introductionmentioning

confidence: 69%

Circ_0001421 facilitates glycolysis and lung cancer development by regulating miR-4677-3p/CDCA3

Zhang

et al. 2020

Diagn Pathol

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Background Lung cancer (LC) is a malignant tumor originating in the bronchial mucosa or gland of the lung. Circular RNAs (circRNAs) are proved to be key regulators of tumor progression. However, the regulatory effect of circ_0001421 on lung cancer tumorigenesis remains unclear. Methods The expression levels of circ_0001421, microRNA-4677-3p (miR-4677-3p) and cell division cycle associated 3 (CDCA3) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Methyl thiazolyl tetrazolium (MTT), Transwell and Tumor formation assays were performed to explore the role of circ_0001421 in LC. Glucose consumption and lactate production were examined by a Glucose assay kit and a Lactic Acid assay kit. Western blot was utilized to examine the protein levels of Hexokinase 2 (HK2) and CDCA3. The interaction between miR-4677-3p and circ_0001421 or CDCA3 was confirmed by dual-luciferase reporter assay. Results Circ_0001421 was increased in LC tissues and cells, and knockdown of circ_0001421 repressed cell proliferation, migration, invasion and glycolysis in vitro. Meanwhile, circ_0001421 knockdown inhibited LC tumor growth in vivo. Mechanistically, circ_0001421 could bind to miR-4677-3p, and CDCA3 was a target of miR-4677-3p. Rescue assays manifested that silencing miR-4677-3p or CDCA3 overexpression reversed circ_0001421 knockdown-mediated suppression on cell proliferation, migration, invasion and glycolysis in LC cells. Conclusion Circ_0001421 promoted cell proliferation, migration, invasion and glycolysis in LC by regulating the miR-4677-3p/CDCA3 axis, which providing a new mechanism for LC tumor progression.

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Section: Introductionmentioning

confidence: 69%

Circ_0001421 facilitates glycolysis and lung cancer development by regulating miR-4677-3p/CDCA3

Zhang

et al. 2020

Diagn Pathol

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“…Researches indicated that depletion of QKI-5 increases cell proliferation and metastasis in oral squamous cell carcinoma, non-small cell lung cancer, renal cell carcinoma and HCC [29,[31][32][33]. What's more, QKI might involve in drug sensitivity.…”

Section: Discussionmentioning

confidence: 99%

LncRNA CCAT1 Enhances Chemoresistance in Hepatocellular Carcinoma by Targeting QKI-5

Shi¹,

Guo²,

Ma³

2020

Preprint

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Background: A major reason for treatment failure of cancer is acquisition of drug resistance. The specific mechanisms underlying hepatocellular carcinoma (HCC) chemoresistance need to be fully elucidated. lncRNAs involve in drug resistance in some cancers, however, the exact functions of lncRNA colon cancer-associated transcript 1 (CCAT1) in oxaliplatin resistance in HCC need to be elucidated.Methods: Functional analysis of CCAT1 on oxaliplatin sensitivity was performed in HCC cell lines HCCLM3 and HepG2, and in a subcutaneous tumor model receiving OXA treatment. Furthermore, the downstream signaling targets of CCAT1 in HCC were explored. Results: CCAT1 promoted HCC proliferation and reduced the apoptosis induced by oxaliplatin. Knockout of CCAT1 could increased chemosensitivity in vitro and in vivo. Further study found that QKI-5 was an important mediator and blocking of QKI-5/p38 MAPK signaling pathway enhanced oxaliplatin sensitivity.Conclusions: CCAT1 promoted proliferation and oxaliplatin resistance by QKI-5/p38 MAPK signaling pathway in HCC. Targeting CCAT1 in combination with chemotherapeutics may be a promising alternative to reverse drug resistance in HCC treatment.

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“…Recently, we found that miR-196b-5p functions as an oncomiRNA in NSCLC by directly targeting GATA6 and TSPAN12 19 . To further validate the oncogenic function of miR-196b-5p in NSCLC, we analyzed miR-196b-5p expression in NSCLC tissues and normal adjacent tissues (NATs) using The Cancer Genome Atlas (TCGA) dataset.…”

Section: Upregulated Mir-196b-5p Inhibits Fas Expression In Nsclcmentioning

confidence: 99%

miR-196b-5p-mediated downregulation of FAS promotes NSCLC progression by activating IL6-STAT3 signaling

et al. 2020

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Our recent study demonstrated that the QKI-5 regulated miRNA, miR-196b-5p, and it functions as an onco-microRNA in non-small cell lung cancer (NSCLC) by directly targeting GATA6 and TSPAN12. However, the role of miR-196b-5p in NSCLC progression and metastasis still remains unclear. We found that miR-196b-5p promotes lung cancer cell proliferation and colony formation by directly targeting tumor suppressor, FAS. The expression of FAS was significantly downregulated in NSCLC tissue samples and was negatively correlated with the miR-196b-5p expression. Knocking down FAS activates NFkB signaling and subsequent IL6 secretion, resulting in phosphorylation of signal transducer and activator of transcription 3 (STAT3) to promote lung cancer cell growth. Our findings indicated that miR-196b-5p might exhibit novel oncogenic function by FAS-mediated STAT3 activation in NSCLC, and suggested that targeting the miR-196b-5p/FAS/NFkB/IL6/STAT3 pathway might be a promising therapeutic strategy in treating NSCLC.

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miR-196b-5p–mediated downregulation of TSPAN12 and GATA6 promotes tumor progression in non-small cell lung cancer

Cited by 128 publications

References 40 publications

Circ_0001421 facilitates glycolysis and lung cancer development by regulating miR-4677-3p/CDCA3

Circ_0001421 facilitates glycolysis and lung cancer development by regulating miR-4677-3p/CDCA3

LncRNA CCAT1 Enhances Chemoresistance in Hepatocellular Carcinoma by Targeting QKI-5

miR-196b-5p-mediated downregulation of FAS promotes NSCLC progression by activating IL6-STAT3 signaling

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