Knockdown of long noncoding RNA urothelial carcinoma associated 1 inhibits colorectal cancer cell proliferation and promotes apoptosis via modulating autophagy

Song, Fengling; Li, Lexing; Liang, Danyang; Zhuo, Yisha; Wang, Xueyi; Dai, Hanchuan

doi:10.1002/jcp.27500

Cited by 30 publications

(20 citation statements)

References 55 publications

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“…LncRNAs were recently demonstrated to play vital roles as major regulators of gene expression and cancer cell proliferation (24) in multiple cancers. Several lncRNAs have been identified as regulators in CRC cell proliferation and metastasis (25). In current study, we focused on a cancer-related lncRNA, LINC00114, which we found to be upregulated in CRC.…”

Section: Discussionmentioning

confidence: 98%

Long Non-coding RNA LINC00114 Facilitates Colorectal Cancer Development Through EZH2/DNMT1-Induced miR-133b Suppression

Chen

et al. 2019

Front. Oncol.

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This study aimed to identify the roles of the long non-coding RNA LINC00114 in colorectal cancer (CRC) development. The expression levels of LINC00114 and miR-133b in CRC were determined by reverse transcription (RT)-polymerase chain reaction (PCR) and the functions of LINC00114 in CRC were evaluated in vitro and in vivo. Methylationspecific PCR assay was performed to detect the miR-133b promoter methylation in CRC cells. Bioinformatics analysis, RNA immunoprecipitation, dual luciferase assay, RNA pull-down, co-immunoprecipitation (IP), and chromatin IP (ChIP) assays were used to elucidate whether LINC00114 could recruit EZH2/DNMT1 and bind to the miR-133b promoter region, leading to dysregulated methylation and the depression of miR-133b. The expression levels of DNA methyltransferases (DNMTs), EZH2, and nucleoporin 214(NUP214) were analyzed by western blotting. Data showed that LINC00114 was highly expressed, whereas miR-133b was downregulated in the CRC tissues and cells. In vitro, silencing LINC00114 inhibited cell proliferation and impeded cell cycle at the G1/S phase by upregulating miR-133b. In vivo, LINC00114 knockdown reduced tumor growth. Further analysis showed that the methylation in miR-133b promoter region was increased in the CRC and silencing LINC00114 increased miR-133b expression through depressing methylation of its promoter region. ChIP-PCR experiments demonstrated that EZH2 and DNMT1 could bind to the miR-133b promoter region and it was abolished by LINC00114 knockdown. sh-EZH2 reversed the overexpression of DNMTs and CRC cell cycle progression induced by the LINC00114 upregulation. LINC00114 could regulate the NUP214 protein expression by sponging miR-133b. These results demonstrated that LINC00114 suppressed miR-133b expression via EZH2/DNMT1-mediated methylation of its promoter region, indicating that LINC00114 might be a potential novel target for CRC diagnosis and treatment.

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Section: Discussionmentioning

confidence: 98%

Long Non-coding RNA LINC00114 Facilitates Colorectal Cancer Development Through EZH2/DNMT1-Induced miR-133b Suppression

Chen

et al. 2019

Front. Oncol.

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“…Instead, autophagy activator RAPA reversed the effect. Therefore, down-regulation of UCA1 induces autophagy inhibition by activating the AKT/mTOR signaling pathway, thereby inhibiting cell proliferation and promoting apoptosis of caco2 cells [ 101 ]. Mounting evidence suggests that LncRNA is a key factor in autophagy [ 102 ].…”

Section: The Main Regulatory Factors Of the Interaction Between Autopmentioning

confidence: 99%

The interaction mechanism between autophagy and apoptosis in colon cancer

Xie

Liu

2020

Translational Oncology

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Autophagy and apoptosis play crucial roles in tumorigenesis. Recent studies have shown that autophagy and apoptosis have a cross-talk relationship in anti-tumor therapy. It is well established that apoptosis is one of the main pathways of tumor cell death. While autophagy can occurs in tumors with opposite function: protective autophagy and lethal autophagy. Protective autophagy can inhibit tumor apoptosis induced by anticancer drugs, while lethal autophagy can induce tumor cell apoptosis in cooperation with anticancer drugs. Hence, autophagy and apoptosis have synergistic and antagonistic effects in tumor. Colorectal cancer is a common malignant tumor with high morbidity and mortality. In recent years, colorectal carcinoma has achieved improved clinical efficacy with drug treatment. Nonetheless, increasing drug-resistance limit the treatment efficacy, highlighting the urgency of exploring the molecular events that drive drug resistance. Researchers have found that autophagy is one of the major factors leading to drug resistance in colon cancer. Therefore, elucidating the interaction between autophagy and apoptosis is helpful to improve the efficacy of anticancer drugs in clinical treatment of colorectal cancer. This review attaches great importance to the relationship between autophagy and apoptosis and related factors in colorectal cancer.

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“…However, in certain settings, UCA1 positively regulates autophagy. For instance, Song et al reported that knockdown of UCA1 inhibited colorectal cancer cell proliferation and promoted apoptosis via suppression of autophagy. Wu et al demonstrated that UCA1 contributed to the progression and drug resistance of bladder cancer cells through ATG7‐mediated induction of autophagy.…”

Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA UCA1 promotes autophagy by targeting miR‐96‐5p in acute myeloid leukaemia

Chen

Wang

et al. 2020

Clin Exp Pharma Physio

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Long non‐coding RNA (lncRNA) urothelial carcinoma‐associated 1 (UCA1) has been identified as an oncogene and is involved in acute myeloid leukaemia (AML). Autophagy contributes to tumourigenesis and cancer cell survival. The purpose of this study was to investigate the regulatory role and mechanism of UCA1 in AML cell viability by its effect on autophagy. The expression of UCA1, miR‐96‐5p, and ATG7 was determined by qRT‐PCR and western blot. Cell proliferation was examined by MTT assay. The autophagy level was assessed by green fluorescent protein (GFP)‐LC3 immunofluorescence and western blot. The interaction between UCA1 and miR‐96‐5p or ATG7 was analyzed by luciferase reporter activity. The results showed that UCA1 promoted AML cell proliferation by inducing autophagy. Mechanistically, UCA1 acted as a sponge of miR‐96‐5p by binding to miR‐96‐5p. ATG7 was a direct target of miR‐96‐5p and positively regulated by UCA1. Further results showed that the miR‐96‐5p mimic effectively counteracted the UCA1 overexpression‐mediated induction of the ATG7/autophagy pathway. Collectively, UCA1 functions as a sponge of miR‐96‐5p to upregulate its target ATG7, thereby resulting in autophagy induction. Our findings reveal a UCA1‐mediated molecular mechanism responsible for autophagy induction in AML and help to improve the understanding of the molecular mechanism of AML progression.

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Knockdown of long noncoding RNA urothelial carcinoma associated 1 inhibits colorectal cancer cell proliferation and promotes apoptosis via modulating autophagy

Cited by 30 publications

References 55 publications

Long Non-coding RNA LINC00114 Facilitates Colorectal Cancer Development Through EZH2/DNMT1-Induced miR-133b Suppression

Long Non-coding RNA LINC00114 Facilitates Colorectal Cancer Development Through EZH2/DNMT1-Induced miR-133b Suppression

The interaction mechanism between autophagy and apoptosis in colon cancer

Long non‐coding RNA UCA1 promotes autophagy by targeting miR‐96‐5p in acute myeloid leukaemia

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