Chen Xi, Xu Wenhui, Shen Yuan, Qi Anning, Qin Huiling
Department of Pathology, Huaihe Hospital of Henan University, Kaifeng, 475000, China.
Department of Pathology, The Second Affiliated Hospital of Naval Medical University, Shanghai, 200003, China.
J Cardiothorac Surg. 2025 Apr 2;20(1):175. doi: 10.1186/s13019-025-03374-1.
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.
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.
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.
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.
作为全球死亡率最高的肿瘤之一,肺腺癌具有较高的隐匿、复发和转移风险,这已成为医学界的一个重大问题。为了寻找肺腺癌可能的治疗靶点,本研究调查了FAM66C与肺腺癌预后的关系及其与miR-339-3p相互作用的机制。
收集117例肺腺癌患者的组织样本和临床病理数据。采用聚合酶链反应法检测肺腺癌组织中FAM66C和miR-339-3p的表达。利用CCK-8、Transwell和流式细胞术评估肺腺癌细胞增殖、迁移、凋亡与FAM66C表达之间的关系。采用双荧光素酶报告基因检测法研究miR-339-3p与FAM66C之间的相互作用。使用卡方检验、Kaplan-Meier法和多因素Cox回归分析评估FAM66C的预后潜力及其与临床病理的关系。
肺腺癌细胞和组织中FAM66C表达显著降低,miR-339-3p表达上调。FAM66C与miR-339-3p呈负相关。FAM66C抑制miR-339-3p的表达,而miR-339-3p可逆转FAM66C对肺腺癌细胞的抑制作用。FAM66c表达与临床TNM分期和淋巴结转移密切相关。当FAM66C表达较低时,肺腺癌患者的预后较差。
总之,较低的FAM66C表达可用于预测肺腺癌的不良预后,且FAM66C与miR-339-3p呈负相关,其可通过调节miR-339-3p表达影响癌细胞的发展。