Knockdown of LncRNA PVT1 inhibits tumorigenesis in non-small-cell lung cancer by regulating miR-497 expression

Guo, Dong; Wang, Yanli; Ren, Kewei; Han, Xinwei

doi:10.1016/j.yexcr.2017.11.014

Cited by 56 publications

(39 citation statements)

References 38 publications

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“…However, miR497 was frequently downregulated in NSCLC 68 and lncPVT1 was considered as the most potential regulator of such phenomenon. 69 Thus, as per available literature, both lncPVT1 and circPVT1 was shown to undergo similar type of molecular alterations in NSCLC and both the candidates seemed to exert an oncogenic effect through common downstream effector by a similar mechanism. Therefore, detailed Review molecular analysis including both lncPVT1 and circPVT1 in the same set of sample is warranted to understand the oncogenic effect exclusive to each candidate in tumorigenesis of lung.…”

Section: Non-small Cell Lung Carcinomamentioning

confidence: 67%

Circular PVT1: an oncogenic non-coding RNA with emerging clinical importance

et al. 2019

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The importance of circular RNAs (circRNAs) in pathological processes like cancer is evident. Among the circRNAs, recent studies have brought circPVT1 under focus as the most potent oncogenic non-coding RNA. Recent studies on various aspects of circPVT1, including its biogenesis, molecular alteration and its probable role in oncogenesis, have been conducted for research and clinical interest. In this review, a first attempt has been made to summarise the available data on circPVT1 from PubMed and other relevant databases with special emphasis on its role in development, progression and prognosis of various malignant conditions. CircPVT1 is derived from the same genetic locus encoding for long non-coding RNA lncPVT1; however, existing literature suggested circPVT1 and lncPVT1 are transcripted independently by different promoters. The interaction between circRNA and microRNA has been highlighted in majority of the few malignancies in which circPVT1 was studied. Besides its importance in diagnostic and prognostic procedures, circPVT1 seemed to have huge therapeutic potential as evident from differential drug response of cancer cell line as well as primary tumors depending on expression level of the candidate. circPVT1 in cancer therapeutics might be promising as a biomarker to make the existing treatment protocol more effective and also as potential target for designing novel therapeutic intervention.

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Section: Non-small Cell Lung Carcinomamentioning

confidence: 67%

Circular PVT1: an oncogenic non-coding RNA with emerging clinical importance

et al. 2019

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“…A growing body of studies have indicated that long noncoding RNAs serve as competing endogenous RNAs during oncogenesis [37]. LncRNA PVT1 is reported to be involved in tumorigenesis and progression of many malignancies, including cervical cancer [38], nonsmall cell lung cancer [39], pancreatic cancer [40], and so forth. In the recent years, some emerging evidence has suggested that silencing PVT1 could inhibit malignant biological behaviors of glioma cells.…”

Section: Discussionmentioning

confidence: 99%

LncRNA PVT1 Facilitates Tumorigenesis and Progression of Glioma via Regulation of MiR-128-3p/GREM1 Axis and BMP Signaling Pathway

Zhang

et al. 2018

Neurotherapeutics

128

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The current research was aimed at probing into the role of long noncoding RNA (lncRNA) PVT1 in the pathogenesis of glioma and the regulatory mechanism of PVT1/miR-128-3p/GREM1 network in glioma via regulation of the bone morphogenetic protein (BMP) signaling pathway. Microarray analysis was used for preliminary screening for candidate lncRNAs and mRNAs in glioma tissues. Real-time quantitative polymerase chain reaction, Western blot, MTT assay, flow cytometry, migration and invasion assays, and xenograft tumor model were utilized to examine the influence of the lncRNA PVT1/miR-128-3p/GREM1 network on the biological functions of glioma cells. Luciferase assay and RNA-binding protein immunoprecipitation assay were used to validate the miR-128-3p-target relationships with lncRNA PVT1 or GREM1. In addition, the impact of GREM1 on BMP signaling pathway downstream proteins BMP2 and BMP4 was detected via Western blot. LncRNA PVT1 was highly expressed in human glioma tissues and significantly associated with WHO grade (I-II vs III-IV; p < 0.05). There existed a regulatory relationship between lncRNA PVT1 and miR-128-3p as well as that between miR-128-3p and GREM1. MiR-128-3p was downregulated, whereas GREM1 was upregulated in glioma tissues in comparison with para-carcinoma tissues. Overexpression of GREM1 promoted the proliferation and metastatic potential of glioma cells, whereas miR-128-3p mimics inhibited the glioma cell activity through targeting GREM1. Furthermore, lncRNA PVT1 acted as a sponge of miR-128-3p and, thus, influenced the BMP signaling pathway downstream proteins BMP2 and BMP4 through regulating GREM1. LncRNA PVT1 modulated GREM1 and BMP downstream signaling proteins through sponging miR-128-3p, thereby promoting tumorigenesis and progression of glioma.

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“…ENST457720 knockout inhibited the proliferation of lung adenocarcinoma cells . Guo et al found increased expression of LncRNA‐PVT1 in nonsmall‐cell lung cancer and LncRNA‐PVT1 directly combined with miR‐497 based on RNA immunoprecipitation assay . LncRNAs could affect the migration capacity of cancer cells through multiple pathways and complex mechanisms.…”

Section: Discussionmentioning

confidence: 99%

“…22 Guo et al found increased expression of LncRNA-PVT1 in nonsmall-cell lung cancer and LncRNA-PVT1 directly combined with miR-497 based on RNA immunoprecipitation assay. 23 LncRNAs could affect the migration capacity of cancer cells through multiple pathways and complex mechanisms. In this study, specific siRNA was transferred into cells in CTP group by transfection reagents.…”

Section: Discussionmentioning

confidence: 99%

LncRNA‐ENST00000501520 promotes the proliferation of malignant‐transformed BEAS‐2B cells induced with coal tar pitch mediated by target genes

Zhang

Meng

et al. 2019

Environmental Toxicology

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As a human carcinogen, coal tar pitch (CTP) can significantly increase the risk of lung cancer. However, the mechanism underlying CTP‐induced lung carcinogenesis has not been well understood. This study aims to explore the role of the LncRNA‐ENST00000501520 in the proliferation of malignant‐transformed human bronchial epithelial cells (BAES‐2B) induced by CTP extract for the first time. BEAS‐2B cells were stimulated with 2.4 μg/mL CTP extract, and then passaged for three times, which were named passage 1 and then passaged until passage 30 (named as CTP group). The ENST000001520 of cells in CTP group was interfered using siRNA. The results showed that ENST000001520 located in cell nucleus (>80%) had no or weak ability of protein encoding. After interference of ENST000001520, the migration and proliferation of cells in CTP group were inhibited, and the cell cycle was arrested in the G0/G1 phase; however, the apoptosis of cells in CTP group was promoted. The target genes (SKB1, CLTB, TAP2, PIPK2, and SOCS3) of ENST000001520 were screened out, and the mRNA and protein expression of SBK1 and SOCS3 was significantly decreased after ENST000001520 interference. SBK1 and SOCS3 may play a promoting role in occurrence and development of cancers. The study suggests that LncRNA‐ENST00000501520 could promote the proliferation in malignant‐transformed BEAS‐2B cells induced with CTP extract which may be mediated by target genes. This study may provide a new target for prevention and treatment of lung cancer.

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Knockdown of LncRNA PVT1 inhibits tumorigenesis in non-small-cell lung cancer by regulating miR-497 expression

Cited by 56 publications

References 38 publications

Circular PVT1: an oncogenic non-coding RNA with emerging clinical importance

Circular PVT1: an oncogenic non-coding RNA with emerging clinical importance

LncRNA PVT1 Facilitates Tumorigenesis and Progression of Glioma via Regulation of MiR-128-3p/GREM1 Axis and BMP Signaling Pathway

LncRNA‐ENST00000501520 promotes the proliferation of malignant‐transformed BEAS‐2B cells induced with coal tar pitch mediated by target genes

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