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1. Shp2 is required in EMT induced by IL-6 in breast cancer cells | |||
Sun Xuan,Zhang Jie,Wang Zhiyong,Ji Wei,Tian Ran,Zhang Fei,Niu Ruifang | |||
Basic Medicine 17 December 2016 | |||
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Abstract:Accumulative evidence demonstrates that protein tyrosine phosphatase Shp2 functions as a powerful tumor promoter in many types of cancers. Abnormal expression of Shp2 has been implicated in many human malignancies. Overexpression of Shp2 in cancer tissues is correlated with cancer metastasis, resistance to targeted therapy, and poor prognosis. The well-known function of Shp2 is its positive role in regulating cellular signaling initiated by growth factors and cytokines, including interleukin-6 (IL-6). Several recent studies have shown that Shp2 is required for epithelial-mesenchymal transition (EMT) triggered by growth factors. However, whether Shp2 is involved in IL-6-signaling-promoted breast cancer EMT and progression remains undefined. In this study, we showed that exogenous and endogenous IL-6 can enhance breast cancer invasion and migration through the promotion of EMT. IL-6 also induces activation of Erk1/2 and phosphorylation of Shp2. Knockdown of Shp2 inhibited IL-6-induced downregulation of E-cadherin, and IL-6 promoted cell migration and invasion. Moreover, by using Shp2 phosphatase mutants, phosphor-tyrosine mimicking, and deficiency mutants, we provided evidence that the phosphatase activity of Shp2 and its tyrosine phosphorylation are necessary for IL-6-induced downregulation of E-cadherin and phosphorylation of Erk1/2. Our findings uncover an important function that links Shp2 to IL-6-promoted breast cancer progression. | |||
TO cite this article:Sun Xuan,Zhang Jie,Wang Zhiyong, et al. Shp2 is required in EMT induced by IL-6 in breast cancer cells[OL].[17 December 2016] http://en.paper.edu.cn/en_releasepaper/content/4714649 |
2. Cryptotanshinone sensitizes Arsenic trioxide-induced Bel-7404 liver cancer cell apoptosis by downregulating phosphorylated-STAT3 in vitro and in vivo | |||
Li Shen,Guangshun Zhang,Zhaohuan Lou,Guanhua Xu,Guangji Zhang | |||
Basic Medicine 25 May 2016 | |||
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Abstract:Background: Arsenic trioxide (ATO) is approved for treating terminal-stage liver cancer in China. Cryptotanshinone (CT), a STAT3 inhibitor, has exhibited certain anti-tumor potency; however, the use of ATO with CT for treating liver cancer has not been reported. Here we try to elucidate how CT could sensitize ATO-induced liver cancer cell apoptosis and examine its correlation with STAT3 in vitro and in vivo. Methods: Cell viabilityof ATO combined with CT was assessed by MTT assay. Cell apoptosis induced by ATO combined with CT was detected by Annexin V/PI staining and apoptosis-related proteins were detected by western blotting. STAT3-related proteins were analysis by western blotting analysis and Immunofluorescence assays. Efficacy evaluation of ATO combined with CT on xenograft was carried in nude mice and related proteins were analysis by Immunohistochemistry assays. Results: First we evaluated cell vitality, and our data indicated that the ATO combined with CT showed obvious growth inhibition of Bel-7404 cells compared to ATO or CT alone. Next we found that ATO combined with CT induced cell apoptosis in Bel-7404 cells and upregulated the activation of apoptosis-related proteins cleaved-caspase-3, cleaved-caspase-9, and cleaved-poly(ADP-ribose) polymerase in a time-dependent manner. Next, we found that ATO combined with CT not only inhibited the constitutive levels of phosphorylated-JAK2 and phosphorylated-STAT3Tyr705 but did so in a time-dependent manner. We also found that ATO combined with CT reversed the upregulated expression of phosphorylated-STAT3Tyr705 stimulated by interleukin-6 and downregulated STAT3 direct target genes and the anti-apoptotic proteins Bcl-2, XIAP, and survivin but obviously upregulated the promoting apoptosis proteins Bax, Bak, and Mcl-1. In vivo studies showed that ATO combined with CT decreased tumor growth. Tumors from ATO combined with CT-treated mice showed decreased levels of phosphorylated-STAT3Tyr705 and the anti-apoptotic protein Bcl-2 but an increased level of pro-apoptotic protein Bax. Conclusions: Our study provides strong evidence of the anti-tumor growth potency of ATO combined with CT and that phosphorylated-STAT3 played a key role in ATO combined with CT-induced liver cancer cell apoptosis. | |||
TO cite this article:Li Shen,Guangshun Zhang,Zhaohuan Lou, et al. Cryptotanshinone sensitizes Arsenic trioxide-induced Bel-7404 liver cancer cell apoptosis by downregulating phosphorylated-STAT3 in vitro and in vivo[OL].[25 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4693550 |
3. Enhanced Colonic Hypersensitivity and Sensitization of Voltage-gated Sodium Channel in Primary Sensory Neurons in Diabetic Rats | |||
Song Zhenyuan,Hu Ji,Zhang Honghong,Xu Guangyin | |||
Basic Medicine 18 May 2015 | |||
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Abstract:Background: Patients with long-standing diabetes often demonstrate intestinal dysfunction and abdominal pain. However, the pathophysiology of abdominal pain in diabetic patients remains elusive. This study was designed to determine roles of voltage-gated sodium channels (VGSCs) in dorsal root ganglion (DRG) in colonic hypersensitivity of diabetic rats. Methods: Diabetic models were induced by a single intraperitoneal injection of Streptozotocin (STZ; 65 mg/kg i.p.) in adult female rats. Behavioral responses to colorectal distention (CRD) were used to determine colonic sensitivity in rats. Colon-specific DRG neurons labeled with DiI were acutely dissociated for measuring excitability and sodium channel currents by whole-cell patch clamp recordings. Western blot analysis was employed to measure the expression of NaV1.7 and NaV1.8 of colon DRGs. Results: STZ injection produced a significantly lower distention threshold than control rats in responding to CRD. STZ injection also depolarized the resting membrane potentials, hyperpolarized action potential threshold, decreased rheobase and increased number of action potentials evoked by 2 and 3 times rheobase stimulation and ramp current stimulation. Furthermore, STZ injection enhanced neuronal sodium current densities of DRG neurons innervating the colon. STZ injection also led to a significant upregulation of NaV1.7 and NaV1.8 expression in colon DRGs compared with age and sex-matched control rats. Conclusion: Our results suggest that enhanced neuronal excitability following STZ injection, which might be mediated by upregulation of NaV1.7 and NaV1.8 expression in primary sensory neurons, may play an important role in diabetic colonic hypersensitivity. | |||
TO cite this article:Song Zhenyuan,Hu Ji,Zhang Honghong, et al. Enhanced Colonic Hypersensitivity and Sensitization of Voltage-gated Sodium Channel in Primary Sensory Neurons in Diabetic Rats[OL].[18 May 2015] http://en.paper.edu.cn/en_releasepaper/content/4644279 |
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