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Your search keyword '"Meng, Ning"' showing total 2 results
2 results on '"Meng, Ning"'

1. Synergistic antitumor activity of regorafenib and lapatinib in preclinical models of human colorectal cancer.

Author

Zhang, Wen-Ji, Li, Yong, Wei, Meng-Ning, Chen, Yao, Qiu, Jian-Ge, Jiang, Qi-Wei, Yang, Yang, Zheng, Di-Wei, Qin, Wu-Ming, Huang, Jia-Rong, Wang, Kun, Zhang, Wen-Juan, Wang, Yi-Jun, Yang, Dong-Hua, Chen, Zhe-Sheng, and Shi, Zhi

Subjects
*REGORAFENIB, *LAPATINIB, *COLON cancer, *COMBINATION drug therapy, *DRUG resistance, *PHARMACOKINETICS, *ANIMAL experimentation, *ANTHROPOMETRY, *ANTINEOPLASTIC agents, *APOPTOSIS, *CELL cycle, *CELL physiology, *CELLS, *DRUG therapy, *COLON tumors, *DRUG synergism, *DOSE-effect relationship in pharmacology, *HETEROCYCLIC compounds, *MICE, *NEOVASCULARIZATION inhibitors, *PYRIDINE, *UREA, *PROTEIN kinase inhibitors, *PATHOLOGIC neovascularization, *PHARMACODYNAMICS, RECTUM tumors
Abstract

Regorafenib significantly prolongs overall survival in patients with metastatic colorectal cancer (mCRC), but the overall clinical efficacy of regorafenib remains quite limited. Combination chemotherapy is a potentially promising approach to enhance anticancer activity, overcome drug resistance, and improve disease-free and overall survival. The current study investigates the antitumor activity of regorafenib in combination with lapatinib in preclinical models of human CRC. Our results show improved antitumor efficacy when regorafenib is combined with lapatinib both in vitro and in vivo. Furthermore, pharmacokinetic analyses revealed that regorafenib and lapatinib do not influence on each plasma concentration. The finding that regorafenib in combination with lapatinib have synergistic activity warrants further clinical investigation of this beneficial combination as a potential treatment strategy for CRC patients. [ABSTRACT FROM AUTHOR]

Published
2017
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2. Regorafenib overcomes chemotherapeutic multidrug resistance mediated by ABCB1 transporter in colorectal cancer: In vitro and in vivo study.

Author

Wang, Yi-Jun, Zhang, Yun-Kai, Zhang, Guan-Nan, Al Rihani, Sweilem B., Wei, Meng-Ning, Gupta, Pranav, Zhang, Xiao-Yu, Shukla, Suneet, Ambudkar, Suresh V., Kaddoumi, Amal, Shi, Zhi, and Chen, Zhe-Sheng

Subjects
*COLON cancer treatment, *REGORAFENIB, *CANCER chemotherapy, *MULTIDRUG resistance, *BIOACCUMULATION, *MEDICAL practice, *IN vitro studies, *ANIMAL experimentation, *ANIMALS, *ANTINEOPLASTIC agents, *BIOLOGICAL models, *CELL lines, *COLON tumors, *DRUG interactions, *DRUG resistance, *DRUG resistance in cancer cells, *CLINICAL drug trials, *EPITHELIAL cells, *GLYCOPROTEINS, *MICE, *PACLITAXEL, *PYRIDINE, *RESEARCH funding, *UREA, *CHEMICAL inhibitors, *PHARMACODYNAMICS, RECTUM tumors
Abstract

Chemotherapeutic multidrug resistance (MDR) is a significant challenge to overcome in clinic practice. Several mechanisms contribute to MDR, one of which is the augmented drug efflux induced by the upregulation of ABCB1 in cancer cells. Regorafenib, a multikinase inhibitor targeting the RAS/RAF/MEK/ERK pathway, was approved by the FDA to treat metastatic colorectal cancer and gastrointestinal stromal tumors. We investigated whether and how regorafenib overcame MDR mediated by ABCB1. The results showed that regorafenib reversed the ABCB1-mediated MDR and increased the accumulation of [3H]-paclitaxel in ABCB1-overexpressing cells by suppressing efflux activity of ABCB1, but not altering expression level and localization of ABCB1. Regorafenib inhibited ATPase activity of ABCB1. In mice bearing resistant colorectal tumors, regorafenib raised the intratumoral concentration of paclitaxel and suppressed the growth of resistant colorectal tumors. But regorafenib did not induce cardiotoxicity/myelosuppression of paclitaxel in mice. Strategy to reposition one FDA-approved anticancer drug regorafenib to overcome the resistance of another FDA-approved, widely used chemotherapeutic paclitaxel, may be a promising direction for the field of adjuvant chemotherapy. This study provides clinical rationale for combination of conventional chemotherapy and targeted anticancer agents. [ABSTRACT FROM AUTHOR]

Published
2017
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