Effect of lncRNA�THOR on proliferation and igration of colon cancer cells

Lv, Ying; Yang, Xiuhua; Wang, Lei

doi:10.3892/ol.2019.10585

Cited by 7 publications

(7 citation statements)

References 21 publications

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“…LncRNA plays an important role in the occurrence and development of cancer [6,8,11,15]. In this study, high expression of LINC00662 was detected in colon cancer tissues and cell lines, and the survival rate of colon cancer patients with high expression of LINC00662 was lower than that of patients with low expression of LINC00662.…”

Section: Discussionmentioning

confidence: 59%

“…Abnormal expression and functions of lncRNA are involved in the occurrence and development of many diseases, especially malignant tumors. It is reported in colon cancer that LINC01082 and lncRNA THOR can regulate cell proliferation, migration and invasion [10,11] . LncRNA can not only directly participate in the posttranscriptional regulation of mRNA, including variable splicing, RNA editing, protein translation and transport, but also affect the expression of target genes by controlling microRNA [12].…”

Section: Introductionmentioning

confidence: 99%

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LncRNA LINC00662 promotes colon cancer tumor growth and metastasis by competitively binding with miR-340-5p to regulate CLDN8/IL22 co-expression and activating ERK signaling pathway

Cheng

Rong

Zhou

et al. 2020

J Exp Clin Cancer Res

102

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Background: LncRNA LINC00662 is closely related to the occurrence and development of cancer. This study aims to explore the effect of LINC00662 on colon cancer tumor growth and metastasis and its molecular mechanism. Methods: CCK8, colony formation, transwell, scratch wound, TUNEL, flow cytometry, RT-PCR, western blotting and immunohistochemistry assays were used to detect the proliferation, apoptosis, invasion and migration of colon cancer cell and mRNA and protein expressions. Luciferase reporter and RNA pull down assays were used to detect the combination of LINC00662 and miR-340-5p or IL22 and the combination of miR-340-5p and CLDN8/IL22. Coimmunoprecipitation were used to detect the co-expression of CLDN8 and IL22 in colon cell lines. The targets of LINC00662 were predicated by Starbase v2.0. The target genes of miR-340-5p were predicated by miRDB and TargetScan. GO and KEGG enrichment analysis were performed by DAVID website. Results: LINC00662 was up-regulation in colon cancer tissues and cell lines. Univariate Cox regression analysis showed that the LINC00662 expression level was related to the poor prognosis. LINC00662-WT and miR-340-5p mimics co-transfection depressed luciferase activity and IL22/CLDN8-WT and miR-340-5p inhibitors co-transfection memorably motivated luciferase activity. LINC00662 overexpression promoted cell proliferation, invasion and migration, and inhibited cell apoptosis in colon cancer. In vivo xenograft studies in nude mice manifested that LINC00662 overexpression prominently accelerate tumor growth. There was an opposite reaction in the biological functions of colon cells and tumor growth between LINC00662 overexpression and LINC00662 inhibition in vitro and in vivo. The functions of miR-340-5p mimics regulating the biological functions of colon cells and tumor growth were consistent with those of LINC00662 inhibition. CLDN8 and IL22, as target genes of miR-340-5p, reversed the functions of LINC00662 affecting the biological functions of colon cells and the protein levels of Bax, Bcl-2, XIAP, VEGF, MMP-2, E-cadherin and N-cadherin. Co-immunoprecipitation experiments indicated that CLDN8 directly interact with IL22 in colon cell lines. LINC00662 regulated CLDN8 and IL22 expressions and the activation of ERK signaling pathway via targeting miR-340-5p. Conclusion: LINC00662 overexpression promoted the occurrence and development of colon cancer by competitively binding with miR-340-5p to regulate CLDN8/IL22 co-expression and activating ERK signaling pathway.

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Section: Discussionmentioning

confidence: 59%

Section: Introductionmentioning

confidence: 99%

LncRNA LINC00662 promotes colon cancer tumor growth and metastasis by competitively binding with miR-340-5p to regulate CLDN8/IL22 co-expression and activating ERK signaling pathway

Cheng

Rong

Zhou

et al. 2020

J Exp Clin Cancer Res

102

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“…The oncogenic role of lncRNA THOR has been determined in liver cancer 54 , 55 , renal carcinoma cells 12 , osteosarcoma 11 , nasopharyngeal carcinoma cells 56 , tongue squamous cells 57 , and colon cancer cells 58 in previous studies. In this study, the h THOR −/− H1299 cell line was generated via CRISPR/Cas9 technology using paired single-guide RNAs (sgRNAs) instead of RNA interference, which is not a complete gene knockout system.…”

Section: Discussionmentioning

confidence: 99%

A novel N6-methyladenosine (m6A)-dependent fate decision for the lncRNA THOR

Yao

et al. 2020

Cell Death Dis

111

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Previous studies have revealed the critical roles of the N6-methyladenosine (m6A) modification of long non-coding RNAs (lncRNAs) in cancers, but the relationship between the oncogenic role of the lncRNA THOR (a representative of cancer/testis lncRNAs) and m6A modification remains unclear. Here, we show that the internal m6A modification of the lncRNA THOR via an m6A-reader-dependent modality regulates the proliferation of cancer cells. Our findings demonstrated that the loss of the lncRNA THOR inhibits the proliferation, migration, and invasion of cancer cells in vitro and in vivo. In addition, m6A is highly enriched on lncRNA THOR transcripts, which contain GA (m6A) CA, GG (m6A) CU, and UG (m6A) CU sequence motifs. RIP-qRT-PCR and RNA pull-down assay results revealed that the specific m6A readers YTHDF1 and YTHDF2 can read the m6A motifs and regulate the stability of the lncRNA THOR (stabilization and decay). These m6A-dependent RNA-protein interactions can maintain the oncogenic role of the lncRNA THOR. Collectively, these findings highlight the critical role of the m6A modification in oncogenic lncRNA THOR and reveal a novel long non-coding RNA regulatory mechanism, providing a new way to explore RNA epigenetic regulatory patterns in the future. Recently, the new field of "RNA epigenetics" has been booming 14,15 , and N6-methyladenosine (m6A) has been identified as a post-transcriptional regulatory mark in multiple RNA species, including messenger RNAs (mRNAs) 1,2,16 , transfer RNAs (tRNAs) 3,4,17-20 , ribosomal RNAs (rRNAs) 21 , small nuclear RNA 22 , small non-coding RNAs (sncRNAs) 23 , and lncRNAs 16,24. It has been reported that the m6A RNA modification is conferred by methyltransferases (writers), such as methyltransferaselike 3 (METTL3), forming the catalytic core of the m6A methyltransferase complex 25-28. In addition, the biological function of m6A is mediated through the recognition of the m6A site by m6A "readers" 1,29,30 , such as the YT521-B homology (YTH) family, including YTH domain

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“…The THOR–IGF2BP1 complex increases the mRNA stability of several proto-oncogenes, including the MYC gene [ 246 ] ( Figure 4 ). Suppression of this lncRNA’s expression leads to decreased proliferation and migration ability of colon cancer cells [ 228 ]. High THOR expression accelerates tumor transformation of retinoblastoma cells [ 258 ] and growth of osteosarcoma, nasopharyngeal, and renal tumors [ 247 , 251 , 257 ].…”

Section: Lncrnamentioning

confidence: 99%

The Role of Non-Coding RNAs in the Regulation of the Proto-Oncogene MYC in Different Types of Cancer

et al. 2021

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Alterations in the expression level of the MYC gene are often found in the cells of various malignant tumors. Overexpressed MYC has been shown to stimulate the main processes of oncogenesis: uncontrolled growth, unlimited cell divisions, avoidance of apoptosis and immune response, changes in cellular metabolism, genomic instability, metastasis, and angiogenesis. Thus, controlling the expression of MYC is considered as an approach for targeted cancer treatment. Since c-Myc is also a crucial regulator of many cellular processes in healthy cells, it is necessary to find ways for selective regulation of MYC expression in tumor cells. Many recent studies have demonstrated that non-coding RNAs play an important role in the regulation of the transcription and translation of this gene and some RNAs directly interact with the c-Myc protein, affecting its stability. In this review, we summarize current data on the regulation of MYC by various non-coding RNAs that can potentially be targeted in specific tumor types.

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Effect of lncRNA�THOR on proliferation and igration of colon cancer cells

Cited by 7 publications

References 21 publications

LncRNA LINC00662 promotes colon cancer tumor growth and metastasis by competitively binding with miR-340-5p to regulate CLDN8/IL22 co-expression and activating ERK signaling pathway

LncRNA LINC00662 promotes colon cancer tumor growth and metastasis by competitively binding with miR-340-5p to regulate CLDN8/IL22 co-expression and activating ERK signaling pathway

A novel N6-methyladenosine (m6A)-dependent fate decision for the lncRNA THOR

The Role of Non-Coding RNAs in the Regulation of the Proto-Oncogene MYC in Different Types of Cancer

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