Wang Shan-Shan, Xie Xin, Wong Chung Sing Timothy, Choi Ying, Fung Ming Chiu
School of Life Sciences, the Chinese University of Hong Kong, Hong Kong, China.
Hepatobiliary Pancreat Dis Int. 2014 Jun;13(3):293-300. doi: 10.1016/s1499-3872(14)60042-4.
Cancer relapse, associated with increased drug resistance and rate of metastasis, often follows completion of chemotherapy but the cancer escape mechanisms are still incompletely understood. Percutaneous ethanol injection (PEI) has been used for treating hepatocellular carcinoma (HCC) for decades, while the recurrence after PEI treatment remains a major limitation. Recent evidence mounted that cancer cells could survive from chemical induced apoptosis, suggesting a potential route through which cancer relapse may occur. This study focuses on the consequence of HepG2 recovery from ethanol-induced apoptotic event.
The model of HepG2 recovery from ethanol-induced apoptotic event was established by live cell imaging, BrdU assay and Western blotting. MTT assay, wound healing assay and invasion assay were used to investigate the behavior of HepG2 after recovery.
HepG2 cells could recover from ethanol-induced apoptosis. These cells changed their behaviors such as drug resistance, mobility and invasiveness. On average, the recovered HepG2 cell clones were found to be 46% more resistant to ethanol and 84% higher in mobility. The recovered clones became 58.2% more sensitive to 5-fluorouracil.
HepG2 cells can recover from ethanol-induced apoptotic event. These cells became more resistant to ethanol and more invasive. Although the recovered cell clones were more resistant to ethanol, they became more sensitive to 5-fluorouracil treatment.
癌症复发常与化疗结束后耐药性增加和转移率上升相关，但癌症逃逸机制仍未完全明确。经皮乙醇注射（PEI）已用于治疗肝细胞癌（HCC）数十年，然而PEI治疗后的复发仍是一个主要限制因素。最近有证据表明癌细胞可从化学诱导的凋亡中存活，提示了癌症复发可能发生的潜在途径。本研究聚焦于HepG2细胞从乙醇诱导的凋亡事件中恢复后的后果。
通过活细胞成像、BrdU检测和蛋白质印迹法建立HepG2细胞从乙醇诱导的凋亡事件中恢复的模型。采用MTT检测、伤口愈合检测和侵袭检测来研究恢复后HepG2细胞的行为。
HepG2细胞能够从乙醇诱导的凋亡中恢复。这些细胞改变了其行为，如耐药性、迁移能力和侵袭性。平均而言，恢复后的HepG2细胞克隆对乙醇的耐药性提高了46%，迁移能力提高了84%。恢复后的克隆对5-氟尿嘧啶的敏感性提高了58.2%。
HepG2细胞能够从乙醇诱导的凋亡事件中恢复。这些细胞对乙醇的耐药性增强且侵袭性增加。尽管恢复后的细胞克隆对乙醇更具耐药性，但它们对5-氟尿嘧啶治疗更敏感。
