Knockdown of TC-1 enhances radiosensitivity of non-small cell lung cancer via the Wnt/β-catenin pathway

Wu, Dapeng; Li, Lei; Yan, Wei

doi:10.1242/bio.017608

Cited by 18 publications

(14 citation statements)

References 29 publications

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“…and EMT in NSCLC via regulating WNT/b-catenin signal [48]. Wu et al revealed that knockdown of TC-1 promoted the susceptibility of NSCLC cells to radiosensitivity via the Wnt/ b-catenin signal [49]. Furthermore, aberrant expression of Wnt1/b-Catenin is considered as an independent poor prognostic marker of NSCLC after surgery [50].…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Repression of lncRNA-SVUGP2 mediated by EZH2 contributes to the development of non-small cell lung cancer via brisking Wnt/β-catenin signal

Wei

Liu

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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To grab the possible impact of lncRNA-SVUGP2 in the biology and process of non-small cell lung cancer (NSCLC). Sixty paired NSCLC tumour and the adjacent non-tumour lung tissues were collected for detection of lncRNA-SVUGP2. lncRNA-SVUGP2 expression in NSCLC cells (SK-MES-1, A549, SPC-A1, and NCI-H1975) was also detected. lncRNA-SVUGP2 was overexpressed and depressed in A549 and H1975 cells, and the effects of lncRNA-SVUGP2 dysregulation on cell biological performances including viability, colony formation, apoptosis, migration and invasion were grabbed. Furthermore, the regulatory association of lncRNA-SVUGP2 vs. EZH2 in H1975 cells, as well as the association between lncRNA-SVUGP2 and Wnt/b-catenin pathway, was explored. lncRNA-SVUGP2 was depressed in NSCLC tissues and cells. Overexpression of lncRNA-SVUGP2 depressed proliferation, induced apoptosis, and suppressed migration and invasion of A549 and H1975 cells. In addition, lncRNA-SVUGP2 was repressed by EZH2 and was inversely correlated with EZH2 levels in H1975 cells. Repression of lncRNA-SVUGP2 potentially participated in the oncogenic function of EZH2. Besides, overexpression of lncRNA-SVUGP2 depressed the briskness of Wnt/b-catenin signal in H1975 cells. Our data reveal that lncRNA-SVUGP2 is under-expressed in NSCLC cells and the reduced expression of lncRNA-SVUGP2 may enhance the development and process of NSCLC by interacting with EZH2 and activating Wnt/b-catenin pathway. ARTICLE HISTORY KEYWORDSNon-small cell lung cancer; lncRNA-SVUGP2; EZH2; Wnt/b-catenin signal CONTACT Sen Wei

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Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Repression of lncRNA-SVUGP2 mediated by EZH2 contributes to the development of non-small cell lung cancer via brisking Wnt/β-catenin signal

Wei

Liu

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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show abstract

“…The Wnt/β-catenin pathway is an important signaling pathway involved in the malignant progression of various tumors, and regulates the proliferation, migration and invasion of cancer cells (17)(18)(19). When Wnt is activated, β-catenin translocates from the cytoplasm to the nucleus and stimulates proto-oncogene cyclin D1 and c-Myc transcription (20,21).…”

Section: Discussionmentioning

confidence: 99%

Suppression of LETM1 by siRNA inhibits cell proliferation and invasion of bladder cancer cells

Huang

Zhang

et al. 2017

Oncology Reports

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The leucine zipper-EF-hand containing transmembrane protein 1 (LETM1) is highly expressed in many human malignancies and is correlated with poor prognosis. However, the function of LETM1 in bladder cancer still remains unknown. In the present study, we analyzed the expression levels of LETM1 in bladder cancer tissues and non-cancerous tissues as well as in four bladder cancer cell lines (T24, EJ, 5637 and J82) and a human bladder epithelial immortalized cell line SV-HUC-1. Small interfering RNA (siRNA) was employed to knockdown the expression of LETM1 in the T24 cells. The proliferation of T24 cells was significantly repressed as evaluated by CCK-8 assays. Transwell migration and invasion assays indicated that knockdown of LETM1 suppressed cell migration and invasion significantly. Flow cytometric analysis revealed that cells had accumulated at the S-phase when the expression of LETM1 was suppressed. Moreover, we found that several oncogenic proteins in the Wnt/β-catenin signaling pathway, namely β-catenin, cyclin D1 and c-Myc were significantly decreased by the LETM1 siRNA. Collectively, these results revealed that the knockdown of LETM1 exhibited tumor suppressive effects, possibly by controlling the downstream Wnt/β-catenin signaling pathway.

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“…Previous research suggests that Wnt/β-catenin pathway may modulate the radiosensitivity of NSCLC cells. For example, knockdown of Thyroid cancer 1 sensitizes NSCLC cell lines to radiotherapy through the Wnt/β-catenin signaling pathway (Wu et al, 2016). In addition, GDK-10017, an inhibitor of the Wnt/ β-catenin signaling pathway, causes significant radiosensitivity of NSCLC cells (Wickham et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Overexpression of Wnt7a enhances radiosensitivity of non-small-cell lung cancer via the Wnt/JNK pathway

et al. 2020

Biology Open

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The Wingless-type protein 7a (Wnt7a) plays an antiproliferative role in non-small-cell lung cancer (NSCLC). Previous studies have indicated that Wnt7a expression was downregulated in radiation-resistant NSCLC cells. However, little is known about its biological functions and molecular mechanisms in radiosensitivity of NSCLC. Thus, NSCLC cell proliferation and apoptosis in response to Wnt7a overexpression and/or radiation were determined by 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyl-tertazolium bromide (MTT) assay and flow cytometry, respectively. The activation of the Wnt/cJun N-terminal kinase (JNK) and Wnt/β-catenin signaling pathways were further examined by western blot in NSCLC cell lines H1650 and A549. Wnt7a overexpression combined with radiation-inhibited cell proliferation and induced apoptosis in NSCLC cell lines compared to Wnt7a overexpression or radiotherapy alone. In addition, the phosphorylation of JNK, but not β-catenin, was congruent with the changes in Wnt7a overexpression and/or radiation. Moreover, the Wnt/JNK pathway could induce the apoptosis of NSCLC cells through the mitochondrial pathway. Inhibition of the Wnt/JNK signaling pathway by SP600125, a JNK inhibitor, contributed to proliferation induction in NSCLC cells. Taken together, these results showed that Wnt7a overexpression sensitized NSCLC cell lines to radiotherapy through the Wnt/JNK signaling pathway.

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Knockdown of TC-1 enhances radiosensitivity of non-small cell lung cancer via the Wnt/β-catenin pathway

Cited by 18 publications

References 29 publications

RETRACTED ARTICLE: Repression of lncRNA-SVUGP2 mediated by EZH2 contributes to the development of non-small cell lung cancer via brisking Wnt/β-catenin signal

RETRACTED ARTICLE: Repression of lncRNA-SVUGP2 mediated by EZH2 contributes to the development of non-small cell lung cancer via brisking Wnt/β-catenin signal

Suppression of LETM1 by siRNA inhibits cell proliferation and invasion of bladder cancer cells

Overexpression of Wnt7a enhances radiosensitivity of non-small-cell lung cancer via the Wnt/JNK pathway

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