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Article

SKIL facilitates tumorigenesis and immune escape of NSCLC via upregulating TAZ/autophagy axis.

Cell death & disease - 2 Dec 2020

Ma Fang, Ding Meng-Ge, Lei Yi-Yu, Luo Li-Hua, Jiang Shun, Feng Yu-Hua, Liu Xian-Ling

Abstract excerpt

Immune escape is an important mechanism in tumorigenesis. The aim of this study was to investigate roles of SKIL in tumorigenesis and immune escape of non-small-cell lung cancer (NSCLC). SKIL expression levels in NSCLC cell line, clinical sample, and adjacent normal tissue were measured by quantitative PCR, western blot, or immunohistochemistry. Lentivirus was used to overexpress/silence SKIL or TAZ expression....

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Identifiers

PMID: 33268765
DOI: 10.1038/s41419-020-03200-7
PMCID: PMC7710697

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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