ArticleJournal of cellular and molecular medicine2020
Linc01014 regulates gefitinib resistance in oesophagus cancer via EGFR-PI3K-AKT-mTOR signalling pathway.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Chaetocin, a Natural Inhibitor of Transketolase, Suppresses the Non-Oxidative Pentose Phosphate Pathway and Inhibits the Growth of Drug-Resistant Non-Small Cell Lung Cancer.Antioxidants (Basel, Switzerland) · 2025Article
- Interplay between lncRNAs and the PI3K/AKT signaling pathway in the progression of digestive system neoplasms (Review).International journal of molecular medicine · 2025Review
- The essential roles of lncRNAs/PI3K/AKT axis in gastrointestinal tumors.Frontiers in cell and developmental biology · 2024Review
- Advances in targeting of miR‑10‑associated lncRNAs/circRNAs for the management of cancer (Review).Oncology letters · 2023Review
- A Pleiotropic Role of Long Non-Coding RNAs in the Modulation of Wnt/β-Catenin and PI3K/Akt/mTOR Signaling Pathways in Esophageal Squamous Cell Carcinoma: Implication in Chemotherapeutic Drug Response.Current oncology (Toronto, Ont.) · 2022Review
- Emerging role of lncRNAs in drug resistance mechanisms in head and neck squamous cell carcinoma.Frontiers in oncology · 2022Review
- Novel Implications of MicroRNAs, Long Non-coding RNAs and Circular RNAs in Drug Resistance of Esophageal Cancer.Frontiers in cell and developmental biology · 2021Review
- Knockdown of NOLC1 Inhibits PI3K-AKT Pathway to Improve the Poor Prognosis of Esophageal Carcinoma.Journal of oncology · 2021Article
- Linc01014 regulates gefitinib resistance in oesophagus cancer via EGFR-PI3K-AKT-mTOR signalling pathway.Journal of cellular and molecular medicine · 2020Article
- Comprehensive analysis ofCancer cell international · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to explore the underlying mechanism of linc01014 in oesophagus cancer gefitinib resistance. Gefitinib-resistant oesophagus squamous cell carcinoma (ESCC gefitinibR) cell lines were constructed by using different gefitinib treatment in FLO-1, KYAE-1, TE-8 and TE-5 cell lines and confirmed by MTS50 and proliferation assays. Expression of linc01014 was overexpressed/silenced in FLO-1 cells followed by gefitinib treatment, and then, the apoptosis-associated markers Bax and Bcl-2, and PI3KCA in PI3K signalling pathway were determined using Western blotting. MST50 and morphology analyses showed that ESCC gefitinibR cell lines presented obvious gefitinib resistance than their parental ESCC cell lines. ESCC gefitinibR cell lines showed significantly higher proliferation abilities than their parental ESCC cell lines after treating with gefitinib. Overexpression of linc01014 significantly inhibited the apoptosis of FLO-1 cells induced by gefitinib and silencing linc01014 obviously promoted the apoptosis of FLO-1 cells induced by gefitinib. Silencing linc01014 could significantly increase the gefitinib chemotherapy sensitivity of oesophagus cancer via PI3K-AKT-mTOR signalling pathway.
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