ArticleCell death & disease2022
m6A methyltransferase METTL3-induced lncRNA SNHG17 promotes lung adenocarcinoma gefitinib resistance by epigenetically repressing LATS2 expression.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 123 citations in OpenAlex.
- The lncRNA-m6A axis in cancer: a bidirectional regulatory network in tumor progression and therapeutic resistance.Journal of translational medicine · 2026Review
- Tumour-macrophage crosstalk initiated by NFIC/METTL3 negative feedback loop via exosomal miR-194-5p promotes NSCLC progression.Clinical and translational medicine · 2026Article
- Expression, functional role, and mechanistic insights into tRF-His-GTG-008 in lung adenocarcinoma.World journal of surgical oncology · 2026Article
- LINC01857 promotes clear cell renal cell carcinoma progression by scaffolding DNMT1 to suppress WIF1 expression.Scientific reports · 2026Article
- Article
- The role of m6A modification in non-small cell lung cancer: functional insights and impact on therapy resistance.Cancer cell international · 2025Review
- ALKBH5 demethylation modification of SE-lncRNA ZMIZ1-AS1 promotes FGFR1-mediated proliferation and invasive metastasis in osteosarcoma.Cellular and molecular life sciences : CMLS · 2025Article
- METTL3-mediated m6A modification of LINC00857 enhances stemness and metastasis of ovarian cancer cells by activating the YAP-TEAD pathway.Scientific reports · 2025Article
- M6A-ALKBH5-dependent RBMS3-AS3 down-regulation suppresses ferroptosis to promote lung adenocarcinoma progression through HNRNPDL/ZEB1/GPX4 axis.NPJ precision oncology · 2025Article
- Screening of PANoptosis regulator-associated long noncoding RNAs and construction of a survival prognostic model in cutaneous melanoma.Translational cancer research · 2025Article
- The inhibitory effect of M2 macrophage-derived exosomes on gefitinib resistant lung adenocarcinoma cells through the MIF/TIMP1/CD74 axis.Scientific reports · 2025Article
- TFAP2C activates PTGES through the NOTCH3 signaling pathway to affect gefitinib resistance in lung adenocarcinoma.Journal of clinical biochemistry and nutrition · 2025Article
- METTL3: a multifunctional regulator in diseases.Molecular and cellular biochemistry · 2025Review
- Reciprocal regulation between m6 A modifications and non-coding RNAs: emerging roles in cancer therapeutic resistance.Discover oncology · 2025Review
- Interactions between long non-coding RNAs and m6 A modification in cancer.Discover oncology · 2025Review
- A METTL3-NFE2L3 axis mediates tumor stemness and progression in lung adenocarcinoma.Science advances · 2025Article
- N6-methyladenosine-mediated upregulation of H19 promotes resistance to bortezomib by modulating the miR-184/CARM1 axis in multiple myeloma.Clinical and experimental medicine · 2025Article
- AL365181.3 as a novel prognostic biomarker for lung adenocarcinoma.Scientific reports · 2025Article
- NCellular and molecular life sciences : CMLS · 2025Article
- Correlation study of LINC02609 and SNHG17 as prognostic biomarkers of kidney renal clear cell carcinoma and therapeutic sensitivity based on public data andFrontiers in immunology · 2025Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gefitinib has been widely applied for the treatment of lung adenocarcinoma (LUAD). However, the long-term application of gefitinib usually leads to acquired drug resistance in tumour patients, resulting in clinical treatment failure. Small nucleolar host gene 17 (SNHG17) has been shown to play a regulatory role in LUAD progression. Nevertheless, the role of SNHG17 in LUAD gefitinib resistance remains elusive. The expression pattern of SNHG17 was examined in tissues and cell lines of gefitinib-sensitive and gefitinib-resistant LUAD, respectively. Gain- and loss-of-function experiments were employed to assess the biological functions of SNHG17 in cell proliferation and apoptosis, as well as aggressive phenotypes of LUAD cells. MeRIP-qPCR and colorimetric quantificational analysis were performed to detect m6A modifications and contents. Fluorescence in situ hybridisation (FISH) and subcellular fractionation analysis were used to reveal the distribution of SNHG17. RIP and ChIP assays were performed to further validate the SNHG17/EZH2/LATS2 regulatory axis. A xenograft tumour growth assay was conducted to evaluate the role of SNHG17 in LUAD gefitinib resistance in vivo. SNHG17 was upregulated in gefitinib-resistant LUAD tissues and cell lines. Functional assays showed that SNHG17 aggravated the malignant phenotypes of gefitinib-resistant LUAD cells. In addition, METTL3-mediated N
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