METTL14 drives growth and metastasis of non-small cell lung cancer by regulating pri-miR-93-5p maturation and TXNIP expression

Qian, Shuai; Liu, Jun; Liao, Wenliang; Wang, Fengping

doi:10.1007/s13258-023-01436-z

Cited by 2 publications

(1 citation statement)

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“…22 A recent study revealed that METTL3 had increased expression in NSCLC, which accelerated NSCLC cell growth and metastasis via the targeting inhibition of FDX1. 23 Moreover, METTL3 had been shown to serve as an oncogene in NSCLC via mediating the m6A modification of antiapoptosis marker Bcl-2 mRNA. 24 Through database analysis, we determined that SF3B4 had abundant m6A methylation sites and METTL3 could interact with SF3B4.…”

Section: Discussionmentioning

confidence: 99%

METTL3‐mediated the m6A modification of SF3B4 facilitates the development of non‐small cell lung cancer by enhancing LSM4 expression

He,

Gu,

Wei

et al. 2024

Thoracic Cancer

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BackgroundSplicing factor B subunit 4 (SF3B4) has been confirmed to participate in the progression of many cancers and is considered to be a potential target for non‐small cell lung cancer (NSCLC). Thus, the role and molecular mechanism of SF3B4 in NSCLC progression deserves further study.MethodsQuantitative real‐time PCR and western blot were employed to detect the mRNA and protein levels of SF3B4, Sm‐like protein 4 (LSM4) and methyltransferase‐like 3 (METTL3). Cell proliferation, apoptosis, invasion, migration and stemness were tested by cell counting kit‐8, colony formation, flow cytometry, transwell, wound healing, and sphere formation assays. The interaction between SF3B4 and METTL3 or LSM4 was confirmed by MeRIP, RIP and Co‐IP assays. Mice xenograft models were constructed to assess the effects of METTL3 and SF3B4 on NSCLC tumorigenesis.ResultsSF3B4 had high expression in NSCLC tissues and was associated with the shorter overall survival of NSCLC patients. Knockdown of SF3B4 suppressed NSCLC cell proliferation, invasion, migration and stemness, while inducing apoptosis. METTL3 promoted SF3B4 mRNA stability by m6A modification, and its knockdown inhibited NSCLC cell growth, metastasis and stemness by downregulating SF3B4. SF3B4 could interact with LSM4, and sh‐SF3B4‐mediated the inhibition on NSCLC cell functions could be reversed by LSM4 overexpression. In addition, reduced METTL3 expression restrained NSCLC tumor growth, and this effect was reversed by SF3B4 overexpression.ConclusionMETTL3‐stablized SF3B4 promoted NSCLC cell growth, metastasis and stemness via positively regulating LSM4.

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Section: Discussionmentioning

confidence: 99%