The Experts below are selected from a list of 327 Experts worldwide ranked by ideXlab platform
Guo Qiang Zhao - One of the best experts on this subject based on the ideXlab platform.
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α solanine enhances the Chemosensitivity of esophageal cancer cells by inducing microrna 138 expression
Oncology Reports, 2018Co-Authors: Jianbo Wu, Wen Qiao Zang, Xinhui Du, Min Li, Yuanyuan Wang, Li Wang, Guo Qiang ZhaoAbstract:: Esophageal cancer is a common malignant tumor worldwide. Inherent and acquired drug resistance are the major challenges faced in anticancer chemotherapy. This study aimed to explore the effects of α-solanine in regards to the Chemosensitivity of esophageal cancer cells. We found that α-solanine enhanced the sensitivity of EC9706 and KYSE30 cells to 5-flurouracil (5-FU) and cisplatin (Cis) by promoting drug-induced apoptosis. qRT-PCR and western blotting results showed that α-solanine treatment promoted miR-138 expression and decreased survivin expression in EC9706 and KYSE30 cells. α-solanine also enhanced the inhibitory effects of 5-Fu and Cis in EC9706 transplanted tumors in mouse models. Dual-Luciferase reporter assay results confirmed survivin as the direct target gene of miR-138. MiR-138 inhibited survivin expression in EC9706 and KYSE30 cells. And miR-138 mimic and si-survivin had similar effects with α-solanine in suppressing survivin expression and promoting cancer cell death. miR-138 inhibitor reversed the Chemosensitivity-enhancing effect of α-solanine. In EC9706 and KYSE30 cells, survivin overexpression rescued the cancer cells from apoptosis caused by α-solanine and miR-138 mimic expression. From these findings, we conclude that α-solanine enhanced the Chemosensitivity of esophageal cancer cells to chemotherapy via the miR-138/survivin pathway. This study provides insight into the molecular mechanism underlying the Chemosensitivity-enhancing function of α-solanine and suggests a new chemotherapeutic strategy for esophageal cancer treatment.
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α-solanine enhances the Chemosensitivity of esophageal cancer cells by inducing microRNA‑138 expression.
Oncology Reports, 2018Co-Authors: Jianbo Wu, Wen Qiao Zang, Xinhui Du, Min Li, Yuanyuan Wang, Li Wang, Guo Qiang ZhaoAbstract:: Esophageal cancer is a common malignant tumor worldwide. Inherent and acquired drug resistance are the major challenges faced in anticancer chemotherapy. This study aimed to explore the effects of α-solanine in regards to the Chemosensitivity of esophageal cancer cells. We found that α-solanine enhanced the sensitivity of EC9706 and KYSE30 cells to 5-flurouracil (5-FU) and cisplatin (Cis) by promoting drug-induced apoptosis. qRT-PCR and western blotting results showed that α-solanine treatment promoted miR-138 expression and decreased survivin expression in EC9706 and KYSE30 cells. α-solanine also enhanced the inhibitory effects of 5-Fu and Cis in EC9706 transplanted tumors in mouse models. Dual-Luciferase reporter assay results confirmed survivin as the direct target gene of miR-138. MiR-138 inhibited survivin expression in EC9706 and KYSE30 cells. And miR-138 mimic and si-survivin had similar effects with α-solanine in suppressing survivin expression and promoting cancer cell death. miR-138 inhibitor reversed the Chemosensitivity-enhancing effect of α-solanine. In EC9706 and KYSE30 cells, survivin overexpression rescued the cancer cells from apoptosis caused by α-solanine and miR-138 mimic expression. From these findings, we conclude that α-solanine enhanced the Chemosensitivity of esophageal cancer cells to chemotherapy via the miR-138/survivin pathway. This study provides insight into the molecular mechanism underlying the Chemosensitivity-enhancing function of α-solanine and suggests a new chemotherapeutic strategy for esophageal cancer treatment.
Timo Schinköthe - One of the best experts on this subject based on the ideXlab platform.
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Determination of caspase-3 activation fails to predict Chemosensitivity in primary acute myeloid leukemia blasts
BMC Cancer, 2005Co-Authors: Peter Staib, Jan Tiehen, Timo Strunk, Timo SchinkötheAbstract:Background Ex-vivo Chemosensitivity tests that measure cell death induction may predict treatment outcome and, therefore, represent a powerful instrument for clinical decision making in cancer therapy. Such tests are, however, work intensive and, in the case of the DiSC-assay, require at least four days. Induction of apoptosis is the mode of action of anticancer drugs and should, therefore, result in the induction of caspase activation in cells targeted by anticancer therapy. Methods To determine, whether caspase activation can predict the Chemosensitivity, we investigated enzyme activation of caspase-3, a key executioner caspase and correlated these data with Chemosensitivity profiles of acute myeloid leukemia (AML) blasts. Results There was, however, no correlation between the ex-vivo Chemosensitivity assessed by measuring the overall rates of cell death by use of the DiSC-assay and caspase-3 activation. Conclusion Thus, despite a significant reduction of duration of the assay from four to one day, induction of apoptosis evaluated by capase-3 activity does not seem to be a valid surrogate marker for Chemosensitivity.
Jugao Fang - One of the best experts on this subject based on the ideXlab platform.
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Pparg may Promote Chemosensitivity of Hypopharyngeal Squamous Cell Carcinoma.
PPAR research, 2020Co-Authors: Meng Lian, Jiaming Chen, Xixi Shen, Lizhen Hou, Jugao FangAbstract:The upregulation of peroxisome proliferator-activated receptor gamma (PPARG) has been shown to increase the Chemosensitivity of several human cancers. This study is aimed at studying if PPARG sensitizes hypopharyngeal squamous cell carcinoma (HSCC) in chemotherapeutic treatments and at dissecting possible mechanisms of observed effects. We integrated large-scale literature data and HSCC gene expression data to identify regulatory pathways that link PPARG and Chemosensitivity in HSCC. Expression levels of molecules within the PPARG regulatory pathways were compared in 21 patients that underwent chemotherapy for primary HSCC, including 12 chemotherapy-sensitive patients (CSP) and 9 chemotherapy-nonsensitive patients (CNSP). In the CPS group, expression levels of PPARG were higher than that in the CNSP group (log-fold-change = 0.50). Structured text mining identified two Chemosensitivity-related regulatory pathways driven by PPARG. In the CSP group, expression levels for 7 Chemosensitivity-promoting genes were increased, while for 13 Chemosensitivity suppressing the gene expression levels were decreased. Our results support the Chemosensitivity-promoting role of PPARG in HSCC tumor cells, most likely by affecting both cell proliferation and cell motility pathways.
Li Meng - One of the best experts on this subject based on the ideXlab platform.
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The clinical significance of in vitro Chemosensitivity test for ovarian cancer
Chinese Journal of Cancer, 2000Co-Authors: Li MengAbstract:Objective: The current study was designed to investigate the clinical significance of in vitro Chemosensitivity test for ovarian cancer. Method: Diphenyltetrazolium bromide(MTT) assay was used to detect Chemosensitivity in vitro for 60 cases of ovarian cancer patients (Stage I, 8 cases;StageⅡ , 2 cases; StageⅢ， 22 cases; StageⅣ , 1 case; recurrence 27). Results: The median in vitro inhibition rates (IRs) of single agent to tumor cells were: Taxol 61.5％ , EADM 52.4％ , Carbo 42.1％ , BLM 33.5％ ,and VCR 10.7％ . The median IRs of combined regimen were: VBP (VCR＋ BLM＋ carboplatin) 79.9％ , VAP (VCR＋ epirubicin＋ carboplatin)75.3％ . The median IRs of VBP and VAP to specific histology of epithelial ovarian cancer(EOC) were 77.3％ and 71.0％ , respectively. The Chemosensitivity test correctly indicated chemotherapy efficacy in 84.6％ of 26 primary evaluable cases with residue tumor of≤ 2 cm. In 15 evaluable of recurrent cases with residue tumor of≤ 2 cm , the 1 year survival rate was 80.0％ of 10 in vitro drug sensitive cases and 37.5％ of 5 in vitro drug resistsnt ones (P 0.05). In 7 cases with residue tumor of 2 cm, only one reached partial response even though they received chemotherapy as indicated by Chemosensitivity test. The 3 year survival rate of 9 patients who had received VBP chemotherapy suggested by Chemosensitivity was 66.7％ , and of 5 patients received VAP treatment,it was 53.3％ . Conclusion: Chemosensitivity is helpful for guiding chemotherapy in ovarian cancer patients. VAP and VBP regimen showed promising effect on epithelial ovarian cancer and deserved to be further studied.
Jianbo Wu - One of the best experts on this subject based on the ideXlab platform.
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α solanine enhances the Chemosensitivity of esophageal cancer cells by inducing microrna 138 expression
Oncology Reports, 2018Co-Authors: Jianbo Wu, Wen Qiao Zang, Xinhui Du, Min Li, Yuanyuan Wang, Li Wang, Guo Qiang ZhaoAbstract:: Esophageal cancer is a common malignant tumor worldwide. Inherent and acquired drug resistance are the major challenges faced in anticancer chemotherapy. This study aimed to explore the effects of α-solanine in regards to the Chemosensitivity of esophageal cancer cells. We found that α-solanine enhanced the sensitivity of EC9706 and KYSE30 cells to 5-flurouracil (5-FU) and cisplatin (Cis) by promoting drug-induced apoptosis. qRT-PCR and western blotting results showed that α-solanine treatment promoted miR-138 expression and decreased survivin expression in EC9706 and KYSE30 cells. α-solanine also enhanced the inhibitory effects of 5-Fu and Cis in EC9706 transplanted tumors in mouse models. Dual-Luciferase reporter assay results confirmed survivin as the direct target gene of miR-138. MiR-138 inhibited survivin expression in EC9706 and KYSE30 cells. And miR-138 mimic and si-survivin had similar effects with α-solanine in suppressing survivin expression and promoting cancer cell death. miR-138 inhibitor reversed the Chemosensitivity-enhancing effect of α-solanine. In EC9706 and KYSE30 cells, survivin overexpression rescued the cancer cells from apoptosis caused by α-solanine and miR-138 mimic expression. From these findings, we conclude that α-solanine enhanced the Chemosensitivity of esophageal cancer cells to chemotherapy via the miR-138/survivin pathway. This study provides insight into the molecular mechanism underlying the Chemosensitivity-enhancing function of α-solanine and suggests a new chemotherapeutic strategy for esophageal cancer treatment.
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α-solanine enhances the Chemosensitivity of esophageal cancer cells by inducing microRNA‑138 expression.
Oncology Reports, 2018Co-Authors: Jianbo Wu, Wen Qiao Zang, Xinhui Du, Min Li, Yuanyuan Wang, Li Wang, Guo Qiang ZhaoAbstract:: Esophageal cancer is a common malignant tumor worldwide. Inherent and acquired drug resistance are the major challenges faced in anticancer chemotherapy. This study aimed to explore the effects of α-solanine in regards to the Chemosensitivity of esophageal cancer cells. We found that α-solanine enhanced the sensitivity of EC9706 and KYSE30 cells to 5-flurouracil (5-FU) and cisplatin (Cis) by promoting drug-induced apoptosis. qRT-PCR and western blotting results showed that α-solanine treatment promoted miR-138 expression and decreased survivin expression in EC9706 and KYSE30 cells. α-solanine also enhanced the inhibitory effects of 5-Fu and Cis in EC9706 transplanted tumors in mouse models. Dual-Luciferase reporter assay results confirmed survivin as the direct target gene of miR-138. MiR-138 inhibited survivin expression in EC9706 and KYSE30 cells. And miR-138 mimic and si-survivin had similar effects with α-solanine in suppressing survivin expression and promoting cancer cell death. miR-138 inhibitor reversed the Chemosensitivity-enhancing effect of α-solanine. In EC9706 and KYSE30 cells, survivin overexpression rescued the cancer cells from apoptosis caused by α-solanine and miR-138 mimic expression. From these findings, we conclude that α-solanine enhanced the Chemosensitivity of esophageal cancer cells to chemotherapy via the miR-138/survivin pathway. This study provides insight into the molecular mechanism underlying the Chemosensitivity-enhancing function of α-solanine and suggests a new chemotherapeutic strategy for esophageal cancer treatment.