ArticleOncoTargets and therapy2020
Silencing of Long Non-Coding RNA Colon Cancer-Associated Transcript 2 Inhibits the Growth and Metastasis of Gastric Cancer Through Blocking mTOR Signaling.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Harnessing the LncRNA CCAT2 role in gastric cancer: from molecular insights to clinical implications.Cancer cell international · 2026Review
- LncRNA CCAT2 promotes malignant progression of metastatic gastric cancer through regulating CD44 alternative splicing.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- Long Non-Coding RNAs (lncRNAs) as Regulators of the PI3K/AKT/mTOR Pathway in Gastric Carcinoma.International journal of molecular sciences · 2023Review
- Eukaryotic initiation factor 5A2 mediates hypoxia-induced autophagy and cisplatin resistance.Cell death & disease · 2022Article
- Gemini Curcumin Suppresses Gastric Cancer AGS Cell Proliferation Through Modulation ofTurkish journal of pharmaceutical sciences · 2022Article
- Inhibition of Musashi-1 enhances chemotherapeutic sensitivity in gastric cancer patient-derived xenografts.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- The Roles of the Colon Cancer Associated Transcript 2 (CCAT2) Long Non-Coding RNA in Cancer: A Comprehensive Characterization of the Tumorigenic and Molecular Functions.International journal of molecular sciences · 2021Review
- Knockdown of long non-coding RNA CCAT2 suppresses growth and metastasis of esophageal squamous cell carcinoma by inhibiting theThe Journal of international medical research · 2021Article
- miR-651-3p Enhances the Sensitivity of Hepatocellular Carcinoma to Cisplatin via Targeting ATG3-Mediated Cell Autophagy.Journal of oncology · 2021Article
- Long Noncoding RNA LIT3527 Knockdown induces Apoptosis and Autophagy through inhibiting mTOR pathway in Gastric Cancer Cells.Journal of Cancer · 2021Article
Corrections and comments
- Retraction · 2022-12-09Author Unresponsive · Concerns/Issues about Data · Concerns/Issues about Image · Duplication of/in Image · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThis study aimed to evaluate the specific role of colon cancer-associated transcript 2 (CCAT2) on gastric cancer (GC), and reveal the potential regulatory mechanism relating to mammalian target of rapamycin (mTOR) signaling.
methodsThe expression of CCAT2 was detected in GC tissues and cells by quantitative real-time PCR (qRT-PCR), and its relation with the pathologic characteristics of GC patients was analyzed. HGC-27 and SGC-7901 cells were transfected with siRNA-CCAT2 to silence CCAT2, and HGC-27 cells were then treated with an mTOR agonist Leucine (Leu) to activate mTOR signaling. The cell proliferation was evaluated by cell viability and colony formation. The cell cycle and apoptosis, and the migration and invasion abilities were detected by Flow cytometry, and Transwell assay, respectively. The expression of PCNA (proliferation marker), Snail, N-cadherin, E-cadherin (invasion markers), P53, Caspase-8, Bcl-2 (apoptosis markers), LC3-II/LC3-I, ATG3, p62 (autophagy makers), phosphorylated mTOR (p-mTOR), p-AKT, and p-p70S6K (mTOR signaling markers) were detected by Western blot.
resultsCCAT2 was upregulated in GC tissues and cells, and positively associated with the maximum tumor diameter, lymphatic metastasis, TNM staging, and low overall survival rate (P < 0.05). siRNA-CCAT2 transfection significantly inhibited the viability, colony formation, and migration and invasion abilities, blocked the cell cycle in G0/G1 phase, and promoted the apoptosis and autophagy of SGC-7901 and HGC-27 cells (P < 0.05). In addition, siRNA-CCAT2 transfection significantly upregulated P53, Caspase-8, LC3-II/LC3-I and ATG3, and downregulated PCNA, Bcl-2, p62, p-mTOR, p-AKT and p-p70S6K in SGC-7901 and HGC-27 cells (P < 0.05). siRNA-CCAT2 reversed the tumor-promoting effect of mTOR signaling activation on HGC-27 cells (P < 0.05).
conclusionSilencing of CCAT2 inhibited the proliferation, migration and invasion, and promoted the apoptosis and autophagy of GC cells through blocking mTOR signaling.
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