Department of Interventional Oncology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Aging (Albany NY). 2024 Sep 12;16(17):12252-12262. doi: 10.18632/aging.206073.
Radiofrequency ablation (RFA) is an established treatment for unresectable and early-stage hepatocellular carcinoma (HCC). However, in some cases, residual tumor cells undergo malignant transformation following RFA. The molecular mechanisms underlying this phenomenon remain poorly understood. EFCAB7, a member of the EF-hand structure family, is of particular interest due to its association with oncogenesis. Nevertheless, the role of EFCAB7 in oncogenesis remains unclear.
Gene expression level of EFCAB7 in HCC tissues before and after RFA was measured, while and experiments were proposed for exploring the roles of EFCAB7 in tumor cell proliferation and metastasis. Mass spectrometry and CO-IP were adopted to validate the interaction between PARK7 and EFCAB7. Finally, PARK7 in EFCAB7 silencing cells was overexpressed and different functions were measured to determine regulation between two genes.
EFCAB7 showed increased expression after RFA in patient samples and EFCAB7 expression correlated with poor prognosis in HCC patients from the TCGA database. Then, EFCAB7 promoted HCC tumor cell proliferation and metastasis while inhibiting apoptosis. Furthermore, Mass spectrometry and Co-IP experiments revealed a direct interaction between EFCAB7 and PARK7. Finally, when we overexpressed PARK7 in EFCAB7 knockdown tumor cells, it rescued proliferation and metastasis, indicating a functional relationship between these two genes.
EFCAB7 might be a core contributor to HCC cells' malignant transformation after RFA and could be a potential novel target to provide a therapeutic strategy for the prevention of recurrence after RFA in HCC.
射频消融（RFA）是治疗不可切除和早期肝细胞癌（HCC）的一种成熟方法。然而，在某些情况下，RFA 后残余肿瘤细胞会发生恶性转化。这种现象的分子机制仍知之甚少。EF 手结构家族的成员 EFCAB7 由于与癌变有关而备受关注。然而，EFCAB7 在癌变中的作用仍不清楚。
测量 HCC 组织在 RFA 前后的 EFCAB7 基因表达水平，并提出和实验，以探讨 EFCAB7 在肿瘤细胞增殖和转移中的作用。采用质谱和 CO-IP 验证 PARK7 和 EFCAB7 之间的相互作用。最后，在 EFCAB7 沉默细胞中过表达 PARK7，并测量不同功能，以确定两个基因之间的调控关系。
EFCAB7 在患者样本中 RFA 后表达增加，并且 TCGA 数据库中 HCC 患者的 EFCAB7 表达与预后不良相关。然后，EFCAB7 促进 HCC 肿瘤细胞增殖和转移，同时抑制细胞凋亡。此外，质谱和 Co-IP 实验揭示了 EFCAB7 和 PARK7 之间的直接相互作用。最后，当我们在 EFCAB7 敲低肿瘤细胞中过表达 PARK7 时，它挽救了增殖和转移，表明这两个基因之间存在功能关系。
EFCAB7 可能是 RFA 后 HCC 细胞恶性转化的核心贡献者，并且可能是预防 HCC 患者 RFA 后复发的潜在新靶点，为提供一种治疗策略。
