Journal of Cardiothoracic Surgery (Apr 2025)

LncRNA FAM66C predicts poor prognosis in patients with lung adenocarcinoma and regulates cell proliferation and metastasis via miR-339-3p

  • Xi Chen,
  • Wenhui Xu,
  • Yuan Shen,
  • Anning Qi,
  • Huiling Qin

DOI
https://doi.org/10.1186/s13019-025-03374-1
Journal volume & issue
Vol. 20, no. 1
pp. 1 – 10

Abstract

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Abstract Background As one of the tumors with the highest fatality rates in the world, LUAD has a high risk of concealment, recurrence, and metastasis, which has turned into a significant issue in the medical community. To find possible treatment targets for LUAD, the study investigated the relationship between FAM66C and the prognosis of LUAD as well as the mechanism by which it interacts with miR-339-3p. Methods Tissue samples and clinicopathological data were collected from 117 LUAD patients. Polymerase chain reaction assay was used to find FAM66C and miR-339-3p expression in LUAD tissues. Utilizing CCK-8, Transwell, and flow cytometry, the relationship between LUAD cell proliferation, migration, apoptosis, and FAM66C expression was assessed. The dual luciferase reporter gene assay was utilized to investigate the interaction between miR-339-3p and FAM66C. The prognostic potential and connection of FAM66C with clinicopathology were evaluated using the Chi-square test, Kaplan-Meier, and multivariate Cox regression analysis. Results FAM66C expression was drastically reduced and miR-339-3p expression was upregulated in LUAD cells and tissues. There was a negative correlation between FAM66C and miR-339-3p. FAM66C inhibits the expression of miR-339-3p, and miR-339-3p can reverse the inhibitory impact of FAM66C on LUAD cells. FAM66c expression was substantially associated with clinical TNM stage and lymph node metastases When FAM66C expression is low, the prognosis of LUAD patients is bad. Conclusions In conclusion, lower FAM66C expression can be utilized to predict the poor prognosis of LUAD, and FAM66C is negatively linked with miR-339-3p, which can influence cancer cell development by modulating miR-339-3p expression.

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