Guavinoside B from Psidium guajava alleviates acetaminophen-induced liver injury via regulating the Nrf2 and JNK signaling pathways

2020 ◽  
Vol 11 (9) ◽  
pp. 8297-8308
Author(s):  
Yuanyuan Li ◽  
Jialin Xu ◽  
Dongli Li ◽  
Hang Ma ◽  
Yu Mu ◽  
...  
Keyword(s):  
Liver Injury ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
Phenolic Compound ◽  
Psidium Guajava ◽  
Jnk Signaling ◽  
Nrf2 Signaling Pathway ◽  
Jnk Signaling Pathway

GUB, a main phenolic compound present in guava fruits, could alleviate APAP-induced liver injury in vitro and in vivo by activating the Nrf2 signaling pathway and inhibiting the JNK signaling pathway.

Ginsenoside Rg1 protects against acetaminophen-induced liver injury via activating Nrf2 signaling pathway in vivo and in vitro

2018 ◽  
Vol 98 ◽  
pp. 58-68 ◽  
Author(s):  
Chenqing Ning ◽  
Xiaoguang Gao ◽  
Changyuan Wang ◽  
Yulong Kong ◽  
Zhihao Liu ◽  
...  
Keyword(s):  
Liver Injury ◽  
Signaling Pathway ◽  
Ginsenoside Rg1 ◽  
Nrf2 Signaling Pathway

scholarly journals Erianin induces G2/M-phase arrest, apoptosis, and autophagy via the ROS/JNK signaling pathway in human osteosarcoma cells in vitro and in vivo

2016 ◽  
Vol 7 (6) ◽  
pp. e2247-e2247 ◽  
Author(s):  
H Wang ◽  
T Zhang ◽  
W Sun ◽  
Z Wang ◽  
D Zuo ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Osteosarcoma Cells ◽  
Jnk Signaling ◽  
Human Osteosarcoma ◽  
Phase Arrest ◽  
Human Osteosarcoma Cells ◽  
M Phase ◽  
Jnk Signaling Pathway

Enhanced tumorigenesis and lymphatic metastasis of CD133+ hepatocarcinoma ascites syngeneic cell lines mediated by JNK signaling pathway in vitro and in vivo

2013 ◽  
Vol 67 (4) ◽  
pp. 337-345 ◽  
Author(s):  
Yanling Jin ◽  
Jun Mao ◽  
Huanxi Wang ◽  
Zhenhuan Hou ◽  
Wei Ma ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Cell Lines ◽  
Lymphatic Metastasis ◽  
Jnk Signaling ◽  
Jnk Signaling Pathway

scholarly journals Overexpressed microRNA-136 works as a cancer suppressor in gallbladder cancer through suppression of JNK signaling pathway via inhibition of MAP2K4

2019 ◽  
Vol 317 (5) ◽  
pp. G670-G681 ◽  
Author(s):  
Jixiang Niu ◽  
Zhen Li ◽  
Fuzhou Li
Keyword(s):  
Gallbladder Cancer ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Nude Mice ◽  
Expression Profiles ◽  
Jnk Signaling ◽  
Jnk Signaling Pathway

In recent studies, microRNAs (miRs) have been widely explored as important regulators in tumor suppression. miR-136 has been suggested to participate in tumor inhibition through control of vital cellular processes, such as angiogenesis, proliferation, and apoptosis. This study aimed to evaluate the effects of overexpressed miR-136 by transferring mimics in gallbladder cancer (GBC) and to assess the functional role of miR-136 in GBC cell behaviors with the involvement of the mitogen-activated protein kinase kinase 4 ( MAP2K4)-dependent JNK signaling pathway. Differentially expressed miRs associated with GBC were screened using microarray expression profiles, which identified that miR-136 expression was decreased in GBC. Furthermore, MAP2K4 was validated as a target gene of miR-136. To uncover functional relevance regarding miR-136 and MAP2K4 in GBC, cultured GBC cell lines were prepared to transfect with mimic, inhibitor, siRNA, or vectors. At the same time, the transfected GBC cells were inoculated into nude mice to validate findings in vivo. The obtained results demonstrated that overexpressed miR-136 inhibited angiogenesis and cell proliferation and promoted apoptosis in GBC cell lines in vitro, accompanied by impeded cellular tumorigenicity in nude mice via the suppression of MAP2K4. Moreover, the overexpression of MAP2K4 and the activation of the JNK signaling pathway reversed the inhibitory effects of miR-136 on the angiogenesis and tumorigenicity of GBC cells. Together, our results indicated that overexpressed miR-136 attenuates angiogenesis and enhances cell apoptosis in GBC via the JNK signaling pathway by downregulating the expression of MAP2K4. NEW & NOTEWORTHY This study is based on previous studies suggesting the tumor-suppressive role of microRNA (miR)-136 in various cancers. We aim to clarify whether miR-136 could function as a tumor suppressor in gallbladder cancer (GBC) and an underlying mechanism. In vitro and in vivo assays delineated that the tumor-suppressive role of miR-136 in GBC is achieved through inactivation of the JNK signaling pathway by downregulation of MAP2K4.

scholarly journals Thapsigargin induces apoptosis in adrenocortical carcinoma by activating endoplasmic reticulum stress and the JNK signaling pathway: an in vitro and in vivo study

2019 ◽  
Vol Volume 13 ◽  
pp. 2787-2798 ◽  
Author(s):  
Lili Wu ◽  
Xuemei Huang ◽  
Yaqi Kuang ◽  
Zengmiao Xing ◽  
Xiujun Deng ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Signaling Pathway ◽  
Adrenocortical Carcinoma ◽  
In Vivo Study ◽  
Jnk Signaling ◽  
Jnk Signaling Pathway

scholarly journals Celastrol induces apoptosis and autophagy via the ROS/JNK signaling pathway in human osteosarcoma cells: an in vitro and in vivo study

2015 ◽  
Vol 6 (1) ◽  
pp. e1604-e1604 ◽  
Author(s):  
H-Y Li ◽  
J Zhang ◽  
L-L Sun ◽  
B-H Li ◽  
H-L Gao ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
In Vivo Study ◽  
Osteosarcoma Cells ◽  
Jnk Signaling ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cells ◽  
Jnk Signaling Pathway

scholarly journals Peiminine Induces G0/G1-Phase Arrest, Apoptosis, and Autophagy via the ROS/JNK Signaling Pathway in Human Osteosarcoma Cells in Vitro and in Vivo

2021 ◽  
Vol 12 ◽  
Author(s):  
Lei Yu ◽  
Yuxi Chen ◽  
Shaohui Yuan ◽  
Yang Cao ◽  
Zhenggang Bi
Keyword(s):  
Signaling Pathway ◽  
Osteosarcoma Cells ◽  
Jnk Signaling ◽  
Human Osteosarcoma ◽  
Phase Arrest ◽  
Human Osteosarcoma Cells ◽  
G1 Phase Arrest ◽  
Jnk Signaling Pathway

Aims: Peiminine has been reported to have various pharmacological properties, including anticancer activity. In this study, we investigated the effect of this alkaloid on osteosarcoma and explored the underlying mechanisms.Methods: To evaluate the antiosteosarcoma effects of peiminine in vitro, cell viability was assessed by CCK-8 and live/dead assays; the effects of the drug on apoptosis and the cell cycle were examined by flow cytometry; the effects on cell migration and invasion were detected by wound healing and Transwell assays, respectively, while its effects on autophagy were observed by transmission electron microscopy and an LC3 fluorescent puncta formation assay. The role of autophagy in the peiminine-mediated effects in osteosarcoma cells was evaluated by CCK-8 assay and western blotting after the application of the autophagy inhibitor chloroquine. The effect of peiminine on reactive oxygen species (ROS) production was analyzed using fluorescence confocal microscopy and spectrophotometry. Additionally, peiminine-treated osteosarcoma cells were exposed to SP600125, a JNK inhibitor, and N-acetylcysteine, a ROS scavenger, after which the contribution of the ROS/JNK signaling pathway to osteosarcoma was assessed using cell viability and LC3 fluorescent puncta formation assays, flow cytometry, and western blotting. A xenograft mouse model of osteosarcoma was generated to determine the antitumor effects of peiminine in vivo.Results: Peiminine suppressed proliferation and metastasis and induced cell cycle arrest, apoptosis, and autophagy in osteosarcoma cells. These anticancer effects of peiminine were found to be dependent on intracellular ROS generation and activation of the JNK pathway. In line with these results, peiminine significantly inhibited xenograft tumor growth in vivo.Conclusions: Peiminine induced G0/G1-phase arrest, apoptosis, and autophagy in human osteosarcoma cells via the ROS/JNK signaling pathway both in vitro and in vivo. Our study may provide an experimental basis for the evaluation of peiminine as an alternative drug for the treatment of osteosarcoma.

scholarly journals Photodynamic therapy induces autophagy-mediated cell death in human colorectal cancer cells via activation of the ROS/JNK signaling pathway

2020 ◽  
Vol 11 (10) ◽  
Author(s):  
Changfeng Song ◽  
Wen Xu ◽  
Hongkun Wu ◽  
Xiaotong Wang ◽  
Qianyi Gong ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Photodynamic Therapy ◽  
Signaling Pathway ◽  
Tumor Promoter ◽  
Human Colorectal Cancer ◽  
In Vivo Models ◽  
Jnk Signaling ◽  
Jnk Signaling Pathway

Abstract Evidence has shown that m-THPC and verteporfin (VP) are promising sensitizers in photodynamic therapy (PDT). In addition, autophagy can act as a tumor suppressor or a tumor promoter depending on the photosensitizer (PS) and the cancer cell type. However, the role of autophagy in m-THPC- and VP-mediated PDT in in vitro and in vivo models of human colorectal cancer (CRC) has not been reported. In this study, m-THPC-PDT or VP-PDT exhibited significant phototoxicity, inhibited proliferation, and induced the generation of large amounts of reactive oxygen species (ROS) in CRC cells. From immunoblotting, fluorescence image analysis, and transmission electron microscopy, we found extensive autophagic activation induced by ROS in cells. In addition, m-THPC-PDT or VP-PDT treatment significantly induced apoptosis in CRC cells. Interestingly, the inhibition of m-THPC-PDT-induced autophagy by knockdown of ATG5 or ATG7 substantially inhibited the apoptosis of CRC cells. Moreover, m-THPC-PDT treatment inhibited tumorigenesis of subcutaneous HCT116 xenografts. Meanwhile, antioxidant treatment markedly inhibited autophagy and apoptosis induced by PDT in CRC cells by inactivating JNK signaling. In conclusion, inhibition of autophagy can remarkably alleviate PDT-mediated anticancer efficiency in CRC cells via inactivation of the ROS/JNK signaling pathway. Our study provides evidence for the therapeutic application of m-THPC and VP in CRC.

Involvement of pregnane X receptor in the suppression of carboxylesterases by metformin in vivo and in vitro, mediated by the activation of AMPK and JNK signaling pathway

2017 ◽  
Vol 102 ◽  
pp. 14-23 ◽  
Author(s):  
Enfang Shan ◽  
Zhu Zhu ◽  
Shuangcheng He ◽  
Dongbao Chu ◽  
Dinghao Ge ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Pregnane X Receptor ◽  
Jnk Signaling ◽  
Jnk Signaling Pathway
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