Evidence map›Paper›PMID 39751722›Full record

ArticleBiochemical genetics2026

FAM107A Inhibits the Growth, Invasion and Aerobic Glycolysis of LUAD Cells by Regulating CRYAB/PI3K/AKT.

Fei Ming, DaiPing Zhang

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In one paragraph

Article in Biochemical genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Fei MingDepartment of the Thoracic Surgery, Hubei Cancer Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 116 Zhuodaoquan South Road, Hongshan District, Wuhan, 430070, Hubei, China. Mingfei_666@163.com.
DaiPing ZhangDepartment of Cardiac Function, Hubei Cancer Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430070, Hubei, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung adenocarcinoma (LUAD) is characterized by its aggressive nature and resistance to treatment. FAM107A is a tumor suppressor gene that has been found to possess inhibitory effects in several cancers, but its role in LUAD remains unclear. This study investigated the role of FAM107A in regulating LUAD cell growth, invasion and aerobic glycolysis and also investigated the potential underlying mechanisms. Our findings revealed that FAM107A is significantly downregulated in LUAD, and its overexpression inhibited LUAD cell growth and invasion. Furthermore, FAM107A overexpression suppressed the anaerobic phase of carbohydrate metabolism in LUAD cells. Mechanistically, FAM107A regulated the CRYAB/PI3K/AKT signaling pathway, thereby inhibiting tumor progression, and similar findings were confirmed in our in vivo mouse model. In conclusion, FAM107A can suppress LUAD progression by regulating the CRYAB/PI3K/AKT pathway and aerobic glycolysis, indicating its potential as therapeutic target for LUAD.

Indexed as

Adenocarcinoma of LungGlycolysisLung NeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAnimalsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansMiceNeoplasm InvasivenessSignal TransductionPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktCarbohydrate metabolismCRYABFAM107ALung adenocarcinoma (LUAD)PI3K/AKT signaling

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.