LncRNA CCAT1 inhibits cell apoptosis of renal cell carcinoma through up-regulation of Livin protein

Chen, Shaoan; Ma, Pengpeng; Li, Bin; Zhu, Dawei; Chen, Xiude; Xiang, Yuzhu; Wang, Tengteng; Ren, Xiangbin; Liu, Chuan; Jin, Xunbo

doi:10.1007/s11010-017-3043-8

Cited by 28 publications

(22 citation statements)

References 22 publications

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“…23 Likely, CCAT1 regulates EGFR expressions in SCC cells. 24 As a fundamental function by IncRNA, CCAT1 can regulate expressions of many miRNAs, including miR-143, miR-155, miR-181a, and miR-218-5p. 24 As a fundamental function by IncRNA, CCAT1 can regulate expressions of many miRNAs, including miR-143, miR-155, miR-181a, and miR-218-5p.…”

Section: Discussionmentioning

confidence: 99%

LncRNA CCAT1 functions as apoptosis inhibitor in podocytes via autophagy inhibition

Yao

Zhao

et al. 2019

J of Cellular Biochemistry

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Podocyte apoptosis importantly contributes to various kidney diseases. Long noncoding RNAs Colon cancer‐associated transcript‐1 (CCAT‐1) has been demonstrated for a critical role in cell proliferation. In the present study, the relationship between CCAT1 and popdocyte impairment, and the underlying mechanism was investigated. Podocytes were isolated from mice and then treated with tumor necrosis factor‐α to simulate podocyte injury. After developed CCAT1 overexpression or knockdown, cell viabilities were determined with the CCK‐8 assay, apoptosis was examined with Flow cytometry, the autophagy was observed by Western blot. Furthermore, phosphorylated PI3K and Akt expressions were examined. We found that after CCAT1 overexpression, the cell viability was significantly increased, apoptosis was significantly decreased, and autophagy was significantly inhibited, which was indicated by induced P62, LC3B‐I and decreased LC3B‐II. In addition, CCAT1 overexpression induced the levels of phosphorylated PI3K and Akt. With Rap treatment, these effects by CCAT1 were reversed. Furthermore, the results contrary to the effects by CCAT1 overexpression were presented after CCAT1 knockdown, and this was inhibited by 3‐MA. Taken together, our results suggested that CCAT1 induction critically participated in apoptosis inhibition in podocytes through autophagy inhibition via increasing PI3K/Akt signaling. This might act as a promising therapeutic intervention for renal diseases associated with podocyte apoptosis.

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Section: Discussionmentioning

confidence: 99%

LncRNA CCAT1 functions as apoptosis inhibitor in podocytes via autophagy inhibition

Yao

Zhao

et al. 2019

J of Cellular Biochemistry

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“…But due to the growing depth of sequencing technology, more and more new lncRNAs have been found to be involved in various physiological and pathological processes [5]. Studies have shown that a number of lncRNAs are abnormally expressed in many tumours and may be involved in multiple processes of tumorigenesis and development, including cell differentiation and proliferation, cell cycle regulation, invasion and metastasis [6][7][8]. Thus, lncRNAs have been regarded as new biomarkers in various cancers including RCC.…”

Section: Introductionmentioning

confidence: 99%

Long intergenic non-coding RNA 1939 eliminates proliferation and migration of human renal cell carcinoma (RCC) cells by down-regulation of miR-154

Zhang

et al. 2020

Artificial Cells, Nanomedicine, and Biotechnology

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Renal carcinoma (RCC) is widely accepted as a malignant tumour of urinary system. Long intergenic non-coding RNA 1939 (LINC01939) is a novel lncRNA which was found to be down-regulated in RCC. Thus, we set out to explore the effect and regulation mechanism of LINC01939 in RCC. LINC01939 and miR-154 in RCC tissues and cell lines were detected using qRT-PCR assay. To examine cellular viability of ACHN and CAKI-1 cells, cell counting kit-8 (CCK-8) assay was exploited here. Flow cytometric analysis was conducted to examine apoptosis. Cell mobility was valued through wound healing assays. Western blotting was applied for examination of proteins related to proliferation, apoptosis, migration and Wnt/ b-catenin/Notch. LINC01939 was down-regulated in RCC tissues. LINC01939 overexpression impeded proliferation and migration, and induced apoptosis. Further study found that the overexpression of LINC01939 strongly suppressed miR-154 expression. Then, the inhibiting effect of overexpressed LINC01939 on proliferation and mobility and the promoting role of LINC01939 in apoptosis were abolished by the combination of miR-154 mimic. Finally, we found that overexpressed LINC01939 inactivated Wnt/b-catenin and Notch through suppressing miR-154. Up-regulation of LINC01939 inhibited proliferation and migration of RCC cells by down-regulating miR-154.

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“…Previous studies revealed that CCAT1 knockdown reduces cell viability in various cancers, including renal cell carcinoma, glioma, melanoma and retinoblastoma [16,[20][21][22]. Herein, CCAT1 expression was knocked down in two GC cell lines and the effects of CCAT1 knockdown on cell viability, colony formation ability and cell cycle progression were investigated.…”

Section: Discussionmentioning

confidence: 98%

Knockdown of long noncoding RNA CCAT1 inhibits cell growth, invasion and peritoneal metastasis via downregulation of Bmi-1 in gastric cancer

Jiang

Fang

et al. 2018

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Long noncoding RNA colon cancer-associated transcript 1 (lncRNA CCAT1) is highly expressed in gastric cancer (GC) tissues compared with normal counterparts and CCAT1 upregulation can promote proliferation and migration of GC cells in vitro. B-cell specific moloney leukemia virus insertion site 1 (Bmi-1) expression is positively correlated with tumor progression. The present study aimed to investigate the biological functions of CCAT1 and the relationships between CCAT1 and Bmi-1 in GC progression. In the present study, CCAT1 was knocked down by specific shRNA transfection in two human GC cell lines (MGC-803 and SGC-7901). The effects of CCAT1 knockdown on GC cell proliferation, cell cycle, migration and invasion were investigated in vitro. The effect of CCAT1 knockdown on peritoneal metastasis was assessed in nude mice. Bmi-1 expression levels were examined both in vitro and in vivo. The results showed that CCAT1 knockdown markedly inhibited cell proliferation, migration and invasion, arrested the cell cycle at G0/G1 phase in vitro, and inhibited peritoneal metastasis in nude mice, along with the downregulation of Bmi-1. Taken together, CCAT1 is functionally involved in growth and metastasis of GC cells and it may be a potential target for GC therapy.

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LncRNA CCAT1 inhibits cell apoptosis of renal cell carcinoma through up-regulation of Livin protein

Cited by 28 publications

References 22 publications

LncRNA CCAT1 functions as apoptosis inhibitor in podocytes via autophagy inhibition

LncRNA CCAT1 functions as apoptosis inhibitor in podocytes via autophagy inhibition

Long intergenic non-coding RNA 1939 eliminates proliferation and migration of human renal cell carcinoma (RCC) cells by down-regulation of miR-154

Knockdown of long noncoding RNA CCAT1 inhibits cell growth, invasion and peritoneal metastasis via downregulation of Bmi-1 in gastric cancer

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