lncRNA AWPPH promotes proliferation and inhibits apoptosis of non‑small cell lung cancer cells by activating the Wnt/β‑catenin signaling pathway

Zhan, Shaoqi; Du, Junfeng; Zhou, Lean; Sun, Baohua

doi:10.3892/mmr.2019.10089

Cited by 17 publications

(29 citation statements)

References 22 publications

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“…Plenty of evidence highlighted that lncRNAs exerted essential roles in various human cancers, such as hepatocellular carcinoma [38], non-small cell lung cancer [39], and epithelial ovarian cancer [40]. It has been testified that lncRNA TMPO-AS1 was an oncogene in prostate cancer [11].…”

Section: Discussionmentioning

confidence: 99%

TMPO-AS1 promotes cell proliferation of thyroid cancer via sponging miR-498 to modulate TMPO

Feng

Zhang

et al. 2020

Cancer Cell Int

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Background: Thyroid cancer (TC) is the most frequent endocrine malignancy. Long noncoding RNAs (lncRNAs) have been confirmed to act as significant roles in tumor development. The role of lncRNA TMPO-AS1 in TC is still unclear, so it remains to be explored. The aim of the research is to investigate the role and regulatory mechanism of TMPO-AS1 in TC. Methods: TMPO-AS1 and TMPO expression in TC tumors and cells was detected by TCGA database and QRT-PCR assay respectively. CCK-8, EDU, TUNEL and western blot assays were conducted to identify the biological functions of TMPO-AS1 in TC. Luciferase reporter and RNA pull down assays were conducted to measure the interaction among TMPO-AS1, TMPO and miR-498. Results: TMPO-AS1 was overexpressed in TC tissues and cell lines. Knockdown of TMPO-AS1 suppressed cell growth and accelerated cell apoptosis in TC. Furthermore, downregulation of TMPO-AS1 suppressed TMPO expression in TC. The data suggested that TMPO expression was upregulated in TC tissues and cell lines and was positively correlated with TMPO-AS1 expression in TC. Furthermore, the expression of miR-498 presented low expression in TC cells. And miR-498 expression was negatively regulated by TMPO-AS1, meanwhile, TMPO expression was negatively regulated by miR-498 in TC cells. Besides, it was confirmed that TMPO-AS1 could bind with miR-498 and TMPO in TC cells. In addition, it was validated that TMPO-AS1 elevated the levels of TMPO via sponging miR-498 in TC cells. Conclusions: TMPO-AS1 promotes cell proliferation in TC via sponging miR-498 to modulate TMPO.

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Section: Discussionmentioning

confidence: 99%

TMPO-AS1 promotes cell proliferation of thyroid cancer via sponging miR-498 to modulate TMPO

Feng

Zhang

et al. 2020

Cancer Cell Int

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“…Long-noncoding RNAs (lncRNAs) was closely related with the development of multiple cancers, such as bladder cancer [3], gastric cancer [4], ovarian cancer [5] and NSCLC [6]. For example, lncRNA LINC-PINT inhibited NSCLC progression by targeting miR-218-5p/PDCD4 [6] and LncRNA AWPPH promoted NSCLC cell proliferation by activating Wnt/β-catenin signaling pathway [7]. LncRNA-XIST served as an oncogene in various cancers [8, 9] and promoted NSCLC development [10–12].…”

Section: Introductionmentioning

confidence: 99%

Downregulation of LncRNA-XIST inhibited development of non-small cell lung cancer by activating miR-335/SOD2/ROS signal pathway mediated pyroptotic cell death

Liu

Yao

Zhang

et al. 2019

Aging

159

130

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LncRNA-XIST participated in the regulation of Non-small cell lung cancer (NSCLC) progression, but the underlying mechanisms are still unclear. This study showed that LncRNA-XIST aberrantly overexpressed in either NSCLC tissues or cell lines comparing to their paired control groups. Knock-down of LncRNA-XIST promoted NSCLC cell apoptosis and inhibited cell proliferation, which were reversed by synergistically treating cells with pyroptosis inhibitor Necrosulfonamide (NSA). In addition, knock-down of LncRNA-XIST also promoted reactive oxygen species (ROS) production and NLRP3 inflammasome activation. In parallel, ROS scavenger N-acetyl cysteine (NAC) abrogated the effects of downregulated LncRNA-XIST on NSCLC cell pyroptosis. Furthermore, miR-335 was the downstream target of LncRNA-XIST and overexpressed LncRNA-XIST increased SOD2 expression levels by sponging miR-335. Mechanistically, miR-335 inhibitor reversed the effects of downregulated LncRNA-XIST on ROS levels and cell pyroptosis, which were abrogated by synergistically knocking down SOD2. Taken together, knock-down of LncRNA-XIST inhibited NSCLC progression by triggering miR-335/SOD2/ROS signal pathway mediated pyroptotic cell death.

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“… 20 For instance, the expression of lncRNA TP73-AS1 was significantly elevated in NSCLC that predicted shorter survival time in patients 21 ; lncRNA AWPPH can facilitate the proliferation of NSCLC cells and suppress the apoptosis. 22 Moreover, lncRNA is also involved in the regulation of radiosensitivity of tumor cells. For instance, lncRNA PVT1 induces radioresistance in NSCLC cells 23 ; high expression of lncRNA GACAT3 can impede metastasis of cancer cells and improve the effect of radiotherapy.…”

Section: Introductionmentioning

confidence: 99%

Long Noncoding RNA PTPRG Antisense RNA 1 Reduces Radiosensitivity of Nonsmall Cell Lung Cancer Cells Via Regulating MiR-200c-3p/TCF4

Niu

Huang

et al. 2020

Technol Cancer Res Treat

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Background: PTPRG antisense RNA 1 has been well-documented to exert an oncogenic role in diverse neoplasms. However, the precise role of PTPRG antisense RNA 1 in regulating radiosensitivity of nonsmall cell lung cancer cells remains largely elusive. Methods: Expression levels of PTPRG antisense RNA 1 and miR-200c-3p in nonsmall cell lung cancer tissues and cells were detected by quantitative real-time polymerase chain reaction, while transcription factor 4 expression was examined by immunohistochemistry and Western blot. After nonsmall cell lung cancer cells were exposed to X-ray with different doses in vitro, Cell Counting Kit -8 assay and colony formation assay were conducted to determine the influence of PTPRG antisense RNA 1 on cell viability. Interaction between miR-200c-3p and PTPRG antisense RNA 1 as well as transcription factor 4 was investigated by dual luciferase reporter assay. Result: In nonsmall cell lung cancer tissues, the expressions of PTPRG antisense RNA 1 and transcription factor 4 were significantly upregulated, whereas the expression of miR-200c-3p was downregulated. It was also proved that PTPRG antisense RNA 1 and 3′-untranslated region of transcription factor 4 can bind to miR-200c-3p. Under X-ray irradiation, overexpressed PTPRG antisense RNA 1 could promote the viability and enhance the radioresistance of nonsmall cell lung cancer cells, and this effect was partially weakened by miR-200c-3p mimics. Transcription factor 4 was identified as a target gene of miR-200c-3p, which could be positively regulated by PTPRG antisense RNA 1. Conclusion: PTPRG antisense RNA 1 reduces the radiosensitivity of nonsmall cell lung cancer cells via modulating miR-200c-3p/TCF4 axis.

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lncRNA AWPPH promotes proliferation and inhibits apoptosis of non‑small cell lung cancer cells by activating the Wnt/β‑catenin signaling pathway

Cited by 17 publications

References 22 publications

TMPO-AS1 promotes cell proliferation of thyroid cancer via sponging miR-498 to modulate TMPO

TMPO-AS1 promotes cell proliferation of thyroid cancer via sponging miR-498 to modulate TMPO

Downregulation of LncRNA-XIST inhibited development of non-small cell lung cancer by activating miR-335/SOD2/ROS signal pathway mediated pyroptotic cell death

Long Noncoding RNA PTPRG Antisense RNA 1 Reduces Radiosensitivity of Nonsmall Cell Lung Cancer Cells Via Regulating MiR-200c-3p/TCF4

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