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2. TNF-α is a potential therapeutic target to overcome sorafenib resistance in hepatocellular carcinomaResearch in context

Author

Wenliang Tan, Xuan Luo, Wenda Li, Jinyi Zhong, Jun Cao, Sicong Zhu, Xianqing Chen, Rui Zhou, Changzhen Shang, and Yajin Chen

Subjects
Medicine, Medicine (General), R5-920
Abstract

Background: The role of tumor necrosis factor alpha (TNF-α) in targeted therapy for hepatocellular carcinoma (HCC) remains largely unknown. The current study aimed to clarify the mechanistic effects of targeting TNF-α to overcome sorafenib resistance in HCC. Methods: A correlation of TNF-α expression with the prognosis was analyzed in 62 HCC patients who underwent surgical resection and subsequent received adjuvant sorafenib treatment. The relation of TNF-α expression and sorafenib sensitivity was determined in different HCC cell lines. The combined therapeutic effects of sorafenib and ulinastatin, which could inhibit TNF-α expression, on HCC were examined in vitro and in vivo. Findings: High TNF-α expression was correlated with poor outcomes in HCC patients who received adjuvant sorafenib after surgery. In vitro experiments showed that TNF-α promotes HCC cell resistant to sorafenib through inducing epithelial-mesenchymal transition (EMT). Notably, the current study revealed that sorafenib has no significant influence on the expression and secretion of TNF-α, and sorafenib had limited effectiveness on reversing EMT in HCC cells with high TNF-α expression. Inhibiting the expression of TNF-α with ulinastatin significantly enhanced the anti-tumor effect of sorafenib on HCC cells with high expression of TNF-α in vitro and in vivo.Interpretation: Our findings indicate that TNF-α may serve as a novel predictor of sorafenib sensitivity in HCC patients. Sorafenib combined with ulinastatin may improve the effectiveness of treatment of HCC in patients with high expression of TNF-α. Fund: This work was supported by grants from the National Natural Science Foundation of China (no.81572398; no.81672419), the Science and Technology Planning Project of Guangdong Province (no. 2017A010105003; no.2015A050502023; no.2016A020216010), and the Natural Science Foundation of Guangdong Province (no.2014A030313061; no. 2013B021800101). Keywords: Hepatocellular carcinoma, Sorafenib resistance, TNF-α, Ulinastatin, Combination treatment

Published
2019
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3. TNF-α is a potential therapeutic target to overcome sorafenib resistance in hepatocellular carcinoma

Author

Jun Cao, Xianqing Chen, Xuan Luo, Jinyi Zhong, Rui Zhou, Wenda Li, Wenliang Tan, Yajin Chen, Sicong Zhu, and Changzhen Shang

Subjects
0301 basic medicine, Research paper, Hepatocellular carcinoma, medicine.medical_treatment, Cell, Targeted therapy, Mice, chemistry.chemical_compound, 0302 clinical medicine, Sorafenib resistance, Liver Neoplasms, General Medicine, Sorafenib, Gene Expression Regulation, Neoplastic, medicine.anatomical_structure, 030220 oncology & carcinogenesis, Female, Tumor necrosis factor alpha, Adjuvant, medicine.drug, Carcinoma, Hepatocellular, Epithelial-Mesenchymal Transition, Models, Biological, General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, Cell Line, Tumor, medicine, Animals, Humans, Protein Kinase Inhibitors, neoplasms, Glycoproteins, Tumor Necrosis Factor-alpha, business.industry, Therapeutic effect, Ulinastatin, medicine.disease, Xenograft Model Antitumor Assays, digestive system diseases, Disease Models, Animal, 030104 developmental biology, chemistry, Drug Resistance, Neoplasm, TNF-α, Combination treatment, Cancer research, business
Abstract

Background The role of tumor necrosis factor alpha (TNF-α) in targeted therapy for hepatocellular carcinoma (HCC) remains largely unknown. The current study aimed to clarify the mechanistic effects of targeting TNF-α to overcome sorafenib resistance in HCC. Methods A correlation of TNF-α expression with the prognosis was analyzed in 62 HCC patients who underwent surgical resection and subsequent received adjuvant sorafenib treatment. The relation of TNF-α expression and sorafenib sensitivity was determined in different HCC cell lines. The combined therapeutic effects of sorafenib and ulinastatin, which could inhibit TNF-α expression, on HCC were examined in vitro and in vivo. Findings High TNF-α expression was correlated with poor outcomes in HCC patients who received adjuvant sorafenib after surgery. In vitro experiments showed that TNF-α promotes HCC cell resistant to sorafenib through inducing epithelial-mesenchymal transition (EMT). Notably, the current study revealed that sorafenib has no significant influence on the expression and secretion of TNF-α, and sorafenib had limited effectiveness on reversing EMT in HCC cells with high TNF-α expression. Inhibiting the expression of TNF-α with ulinastatin significantly enhanced the anti-tumor effect of sorafenib on HCC cells with high expression of TNF-α in vitro and in vivo. Interpretation: Our findings indicate that TNF-α may serve as a novel predictor of sorafenib sensitivity in HCC patients. Sorafenib combined with ulinastatin may improve the effectiveness of treatment of HCC in patients with high expression of TNF-α. Fund This work was supported by grants from the National Natural Science Foundation of China (no.81572398; no.81672419), the Science and Technology Planning Project of Guangdong Province (no. 2017A010105003; no.2015A050502023; no.2016A020216010), and the Natural Science Foundation of Guangdong Province (no.2014A030313061; no. 2013B021800101).

Published
2019

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