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

Li, N; Jiang, Kui; Fang, Liping; Yao, Lulu; Yu, Zujiang

doi:10.4149/neo_2018_171206n801

Cited by 21 publications

(20 citation statements)

References 33 publications

(44 reference statements)

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“…Examination of the expression of lncRNAs during TNF- α induced osteogenic differentiation revealed 58 upregulated and 19 downregulated lncRNAs on day 7 and 73 upregulated and 60 downregulated lncRNAs on day 14 [ 181 ]. lncRNA colon cancer-associated transcript 1 (CCAT1) is initially discovered to participate in metabolic, migratory, and proliferative processes in some cancers [ 182 ]. Later on, it was found that CCAT1 can promote the proliferation and odontogenic differentiation of DPSCs.…”

Section: Epigenetic Mechanisms In Dpscsmentioning

confidence: 99%

Epigenetic Regulation of Dental Pulp Stem Cell Fate

Zhou

Gan

Yan

et al. 2020

Stem Cells International

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Epigenetic regulation, mainly involving DNA methylation, histone modification, and noncoding RNAs, affects gene expression without modifying the primary DNA sequence and modulates cell fate. Mesenchymal stem cells derived from dental pulp, also called dental pulp stem cells (DPSCs), exhibit multipotent differentiation capacity and can promote various biological processes, including odontogenesis, osteogenesis, angiogenesis, myogenesis, and chondrogenesis. Over the past decades, increased attention has been attracted by the use of DPSCs in the field of regenerative medicine. According to a series of studies, epigenetic regulation is essential for DPSCs to differentiate into specialized cells. In this review, we summarize the mechanisms involved in the epigenetic regulation of the fate of DPSCs.

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Section: Epigenetic Mechanisms In Dpscsmentioning

confidence: 99%

Epigenetic Regulation of Dental Pulp Stem Cell Fate

Zhou

Gan

Yan

et al. 2020

Stem Cells International

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“…Overexpression of CCAT1 has been observed in colorectal cancer, where it promotes tumor growth and metastasis [22, 23]. Similarly, CCAT1 is overexpressed in gastric cancer tissue and is associated with tumor progression [24, 25]. One study has demonstrated an association between CCAT1 and both overall and progression-free survival in breast cancer [26].…”

Section: Introductionmentioning

confidence: 99%

CCAT1 promotes triple-negative breast cancer progression by suppressing miR-218/ZFX signaling

Han

Fan

et al. 2019

Aging

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Long non-coding RNAs (lncRNAs) regulate cancer development and progression. Here, we investigated the role of the lncRNA CCAT1 in triple-negative breast cancer (TNBC). CCAT1 expression was higher in TNBC cells than normal breast epithelial cells. Additionally, CCAT1 expression was higher in TNBC patient tumor tissue than adjacent normal breast tissue. Silencing CCAT1 inhibited TNBC cell proliferation, migration, and invasion in vitro , and tumor growth and progression in vivo . Bioinformatics analysis revealed that microRNA-218 (miR-218) is a potential target of CCAT1. Silencing CCAT1 resulted in an increase in miR-218 expression and inhibited TNBC cell proliferation, migration, and invasion. Silencing miR-218 reversed the effects of CCAT1 knockdown on cell proliferation, migration, and invasion, suggesting that CCAT1 promotes TNBC progression by downregulating miR-218 expression. We identified the zinc finger protein ZFX as a putative downstream target of miR-218 through bioinformatics analysis. ZFX expression was higher in TNBC than normal breast cell lines and higher in TNBC tumor tissue than adjacent normal breast tissue. Overexpression of ZFX reversed the tumor-suppressive effects of miR-218 on TNBC cell proliferation, migration, and invasion. Our data indicate that CCAT1 promotes TNBC progression by targeting the miR-218/ZFX axis.

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“…Dong et al reported that CCAT1 was significantly upregulated in nasopharyngeal carcinoma (NPC) tissues and that CCAT1 induced growth, migration and invasion and inhibited apoptosis in NPC cells [30]. Li et al also found that CCAT1 was highly expressed in gastric cancer (GC) tissues compared with normal counterparts and that CCAT1 upregulation promoted proliferation, invasion and migration of GC cells in vitro [31]. Another study demonstrated that CCAT1 was significantly upregulated in multiple myeloma (MM) tissues and cell lines and that CCAT1 knockdown significantly inhibited cell proliferation, induced cell cycle arrest at the G0/G1 phase, promoted cell apoptosis in vitro, and suppressed tumor growth in vivo [32].…”

Section: Discussionmentioning

confidence: 99%

Downregulation of lncRNA CCAT1 enhances 5-fluorouracil sensitivity in human colon cancer cells

Yang

Pan

Deng

2019

BMC Mol and Cell Biol

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Background The purpose of this study was to determine the aberrant expression of the long noncoding RNA (lncRNA) colon cancer-associated transcript 1 (CCAT1) in 5-fluorouracil-resistant colonic neoplasm cells and to elucidate its effects on the 5-fluorouracil sensitivity of human colonic neoplasm cells. The aberrant expression of lncRNAs in normal tissues and colonic neoplasm tissues was detected by microarray assay. qRT-PCR analysis was performed to assess CCAT1 expression levels in colonic neoplasm cell lines and corresponding normal tissues. After constructing the 5-FU-resistant cell lines and validating the resistance by measuring the IC 50 value, the CCAT1 expression levels in parental and artificially resistant cell lines were determined by qRT-PCR. Transfection was used to modulate the expression of CCAT1. Cell proliferation and apoptosis were then detected by CCK-8 and flow cytometry, respectively. Results CCAT1 in colon cancer tissues was higher than that in noncancer tissues, and the levels of CCAT1 in HCT 116, SW1417, HT-29, and KM12 cell lines were higher than those in the human normal colon epithelial NCM460 cell line. Moreover, the expression levels of CCAT1 were high in HCT 116/5-FU and HT-29/5-FU cell lines, whose apoptosis rates induced by 5-FU were lower than those in corresponding parental cells. The results of qRT-PCR and CCK-8 assay showed that enhancement of lncRNA CCAT1 expression levels in HCT 116 and HT-29 cell lines increased their IC 50 of 5-FU and decreased their apoptosis rates. Meanwhile, siRNA-CCAT1 effectively inhibited the expression of CCAT1 and enhanced the 5-FU-sensitivity of HCT 116/5-FU and HT-29/5-FU, in which apoptosis rates were increased at the same time. Conclusions Downregulation of CCAT1 effectively reversed the resistance of HCT 116/5-FU and HT-29/5-FU cells to 5-FU chemotherapeutic, opening a new avenue in colon cancer therapy.

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

Cited by 21 publications

References 33 publications

Epigenetic Regulation of Dental Pulp Stem Cell Fate

Epigenetic Regulation of Dental Pulp Stem Cell Fate

CCAT1 promotes triple-negative breast cancer progression by suppressing miR-218/ZFX signaling

Downregulation of lncRNA CCAT1 enhances 5-fluorouracil sensitivity in human colon cancer cells

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