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pmid:36494339

Gene amplification-driven lncRNA SNHG6 promotes tumorigenesis via epigenetically suppressing p27 expression and regulating cell cycle in non-small cell lung cancer.

Qi Wang · Wei Zhang · Dandan Yin · Zaibin Tang · Erbao Zhang · Weibing Wu

Cell death discovery · 2022 doi:10.1038/s41420-022-01276-y

Paper

complete

Experiment

complete

Data

partial

Analysis

complete

Execution

absent

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Record details sci_version · id · kind · revision · content_hash · schema · created_at · updated_at · generator
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pmid:36494339
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science-record
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sha256:b31300551df02929b7dc346283db749aef222fa1c4c532c7aa16cdbb4e301a52
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2026-11-01T19:00:59Z
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2026-11-01T21:29:38Z
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complete
title
Gene amplification-driven lncRNA SNHG6 promotes tumorigenesis via epigenetically suppressing p27 expression and regulating cell cycle in non-small cell lung cancer.
doi
10.1038/s41420-022-01276-y
pmid
36494339
authors array · 6 items
[0]
Qi Wang
[1]
Wei Zhang
[2]
Dandan Yin
[3]
Zaibin Tang
[4]
Erbao Zhang
[5]
Weibing Wu
journal
Cell death discovery
year
2022
abstract
Long non-coding RNAs (lncRNAs) have been validated to play essential roles in non-small cell lung carcinoma (NSCLC) progression. In this study, through systematically screening GSE33532 and GSE29249 from Gene Expression Omnibus (GEO) database and bioinformatics analysis, we found the significant upregulation of SNHG6 in NSCLC. The activation of SNHG6 was driven by copy number amplification and high expression of SNHG6 indicated a poor prognosis. Functionally, the knockdown of SNHG6 inhibited NSCLC cell proliferation, migration, and suppressed the G1/S transition of the cell cycle. SNHG6 overexpression had the opposite effects. Mechanically, SNHG6 recruited EZH2 to the promoter region of p27 and increased H3K27me3 enrichment, thus epigenetically repressing the expression of p27, regulating the cell cycle, and promoting tumorigenesis of NSCLC. SNHG6 silencing restrained tumor growth in vivo and suppressed the expressions of cell cycle-related proteins in the G1/S transition. In conclusion, our study uncovered a novel mechanism of SNHG6 activation and its function. SNHG6 can be considered a potential target for the diagnosis and treatment of NSCLC in the future.
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Differential expression analysis and statistical significance of differences between the different groups were performed using unpaired student’s t-test and the data passed normal distribution detection. Kaplan–Meier method and log-rank test were adopted to evaluate the associations between SNHG6/p27 expression and NSCLC prognosis.
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sections[22] "Statistical analysis" paragraph 2
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Differential expression analysis and statistical significance of differences between the different groups were performed using unpaired student’s t-test and the data passed normal distribution detection. Kaplan–Meier method and log-rank test were adopted to evaluate the associations between SNHG6/p27 expression and NSCLC prognosis.
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The data underlying this article will be shared on reasonable request to the corresponding author.
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SNHG6 expression was positively correlated with its copy number in NSCLC (P < 0.001, r = 0.52, n = 989).
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SNHG6 expression was positively correlated with its copy number in NSCLC (Fig. 1h, P < 0.001, r = 0.52, n = 989).
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sections[3] "Gene amplification-driven SNHG6 was aberrantly upregulated in NSCLC, which predicated a poorer prognosis" paragraph 4
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SNHG6 expression was positively correlated with its copy number in NSCLC (Fig. 1h, P < 0.001, r = 0.52, n = 989).
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SNHG6 expression was positively correlated with its copy number in NSCLC (P < 0.001, r = 0.52, n = 989).
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Genome-wide analysis of gene expression in Non-small Cell Lung Cancer
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Intratumor heterogeneity of gene expression profiles in early stage non-small cell lung cancer (NSCLC)
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Differential expression analysis and statistical significance of differences between the different groups were performed using unpaired student’s t-test and the data passed normal distribution detection. Kaplan–Meier method and log-rank test were adopted to evaluate the associations between SNHG6/p27 expression and NSCLC prognosis.
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ndicated a poor prognosis. Functionally, the knockdown of SNHG6 inhibited NSCLC cell proliferation,
[1]
opti-MEM medium (Gibco, Rockville, USA). The transfection by the lentivirus vector was detailed in the
[2]
Animal experiment We constructed the stably transfected A549 cell lines with shSNHG6 and negative co
[3]
esized by GENECHEM (Shanghai, China) and the transfection was performed according to the instructions
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CLC. SNHG6 silencing restrained tumor growth in vivo and suppressed the expressions of cell cycle
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r)2/2 every 3 days. On the 15th day, all the mice were euthanized and the tumors were taken out for
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th shSNHG6 and negative control (shCtrl) for in vivo experiments. The lentivirus-coated shRNAs co
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Science Academy. SPCA1, PC9, and 16HBE were cultured in Dulbecco’s modified Eagle’s medium (DMEM) (G
[1]
re and transfections Human NSCLC cell lines (A549, SPCA1, H1299, H1975, and PC9) and human bro
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aformaldehyde for hematoxylin-eosin (HE) and Ki-67 staining. This study was performed according
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Differential expression analysis and statistical significance of differences between the different groups were performed using unpaired student’s t-test and the data passed normal distribution detection. Kaplan–Meier method and log-rank test were adopted to evaluate the associations between SNHG6/p27 expression and NSCLC prognosis.
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Complete file
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In this study, through systematically screening GSE33532 and GSE29249 from Gene Expression Omnibus (GEO) database and bioinformatics analysis, we found the significant upregulation of SNHG6 in NSCLC. The activation of SNHG6 was driven by copy number amplification and high expression of SNHG6 indicated a poor prognosis. Functionally, the knockdown of SNHG6 inhibited NSCLC cell proliferation, migration, and suppressed the G1/S transition of the cell cycle. SNHG6 overexpression had the opposite effects. Mechanically, SNHG6 recruited EZH2 to the promoter region of p27 and increased H3K27me3 enrichment, thus epigenetically repressing the expression of p27, regulating the cell cycle, and promoting tumorigenesis of NSCLC. SNHG6 silencing restrained tumor growth in vivo and suppressed the expressions of cell cycle-related proteins in the G1/S transition. In conclusion, our study uncovered a novel mechanism of SNHG6 activation and its function. SNHG6 can be considered a potential target for the diagnosis and treatment of NSCLC in the future.", "claims": [{"id": "claim-method", "statement": "Differential expression analysis and statistical significance of differences between the different groups were performed using unpaired student’s t-test and the data passed normal distribution detection. Kaplan–Meier method and log-rank test were adopted to evaluate the associations between SNHG6/p27 expression and NSCLC prognosis.", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:36494339", "locator": "sections[22] \"Statistical analysis\" paragraph 2", "quote": "Differential expression analysis and statistical significance of differences between the different groups were performed using unpaired student’s t-test and the data passed normal distribution detection. Kaplan–Meier method and log-rank test were adopted to evaluate the associations between SNHG6/p27 expression and NSCLC prognosis."}], "state": "complete"}, {"id": "claim-data-access", "statement": "The data underlying this article will be shared on reasonable request to the corresponding author.", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:36494339", "locator": "sections[29] \"notes\" paragraph 1", "quote": "The data underlying this article will be shared on reasonable request to the corresponding author."}], "state": "complete"}, {"id": "claim-target-result", "statement": "SNHG6 expression was positively correlated with its copy number in NSCLC (P < 0.001, r = 0.52, n = 989).", "kind": "quantitative", "target": {"value": 0.52, "unit": "correlation coefficient", "tolerance": null, "source": "SNHG6 expression was positively correlated with its copy number in NSCLC (Fig. 1h, P < 0.001, r = 0.52, n = 989)."}, "evidence": [{"asset": "source:pmid:36494339", "locator": "sections[3] \"Gene amplification-driven SNHG6 was aberrantly upregulated in NSCLC, which predicated a poorer prognosis\" paragraph 4", "quote": "SNHG6 expression was positively correlated with its copy number in NSCLC (Fig. 1h, P < 0.001, r = 0.52, n = 989)."}], "state": "complete"}], "gaps": []}, "experiment": {"state": "complete", "objective": "SNHG6 expression was positively correlated with its copy number in NSCLC (P < 0.001, r = 0.52, n = 989).", "steps": [{"id": "read_published_estimate", "order": 1, "name": "Read the published estimate from the source", "kind": "other", "state": "complete", "blocked_on": null, "description": "The claim, method and evidence span published with the source article.", "duration_hours": null, "parameters": {}, "inputs": ["source:pmid:36494339"], "outputs": ["the published estimate and its evidence"], "instruments": [], "reagents": []}, {"id": "obtain_source_data", "order": 2, "name": "Obtain the source data from the named repository", "kind": "data-preparation", "state": "complete", "blocked_on": null, "description": "The GEO series accession resolves and its sample accessions are listed. 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Functionally, the knockdown of SNHG6 inhibited NSCLC cell proliferation,", "opti-MEM medium (Gibco, Rockville, USA). The transfection by the lentivirus vector was detailed in the", "Animal experiment We constructed the stably transfected A549 cell lines with shSNHG6 and negative co", "esized by GENECHEM (Shanghai, China) and the transfection was performed according to the instructions"], "order_basis": "paper_text_order:588", "id": "assay:1"}, {"role": "data_generation", "definition_id": "animal_model", "definition_version": "99e1195c7d6f", "definition_digest": null, "required_operations": [], "support_state": "partial", "source_hashes": {"assay_lexicon": "99e1195c7d6f"}, "confidence": 0.99, "evidence": ["CLC. SNHG6 silencing restrained tumor growth in vivo and suppressed the expressions of cell cycle", "r)2/2 every 3 days. On the 15th day, all the mice were euthanized and the tumors were taken out for", "th shSNHG6 and negative control (shCtrl) for in vivo experiments. The lentivirus-coated shRNAs co"], "order_basis": "paper_text_order:1014", "id": "assay:2"}, {"role": "data_generation", "definition_id": "cell_culture", "definition_version": "99e1195c7d6f", "definition_digest": null, "required_operations": [], "support_state": "partial", "source_hashes": {"assay_lexicon": "99e1195c7d6f"}, "confidence": 0.99, "evidence": ["Science Academy. SPCA1, PC9, and 16HBE were cultured in Dulbecco’s modified Eagle’s medium (DMEM) (G", "re and transfections Human NSCLC cell lines (A549, SPCA1, H1299, H1975, and PC9) and human bro", "cillin-Streptomycin (Gibco, Rockville, USA). A549, H1299, and H1975 were incubated in Roswell", "riment We constructed the stably transfected A549 cell lines with shSNHG6 and negative control"], "order_basis": "paper_text_order:1375", "id": "assay:3"}, {"role": "data_generation", "definition_id": "ihc", "definition_version": "99e1195c7d6f", "definition_digest": null, "required_operations": [], "support_state": "partial", "source_hashes": {"assay_lexicon": "99e1195c7d6f"}, "confidence": 0.85, "evidence": ["aformaldehyde for hematoxylin-eosin (HE) and Ki-67 staining. 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