Metformin attenuates cadmium-induced neuronal apoptosis in vitro via blocking ROS-dependent PP5/AMPK-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.

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microRNA-195 attenuates neuronal apoptosis in rats with ischemic stroke through inhibiting KLF5-mediated activation of the JNK signaling pathway

Molecular Medicine ◽

10.1186/s10020-020-00150-w ◽

2020 ◽

Vol 26 (1) ◽

Cited By ~ 4

Author(s):

Lisha Chang ◽

Wan Zhang ◽

Songxin Shi ◽

Yanbo Peng ◽

Dali Wang ◽

...

Keyword(s):

Ischemic Stroke ◽

Signaling Pathway ◽

Neuronal Apoptosis ◽

Jnk Signaling ◽

Jnk Signaling Pathway

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hCG Improves Luteal Function and Promotes Progesterone Output through the Activation of JNK Pathway in the Luteal Granulosa Cells of the Stimulated IVF Cycles†

Biology of Reproduction ◽

10.1093/biolre/ioaa034 ◽

2020 ◽

Vol 102 (6) ◽

pp. 1270-1280 ◽

Cited By ~ 3

Author(s):

Gamze Bildik ◽

Nazli Akin ◽

Yashar Esmaeilian ◽

Francesko Hela ◽

Kayhan Yakin ◽

...

Keyword(s):

Luteinizing Hormone ◽

Signaling Pathway ◽

Granulosa Cells ◽

Luteal Phase ◽

Steroidogenic Enzymes ◽

Jnk Pathway ◽

Jnk Signaling ◽

Luteal Function ◽

Jnk Signaling Pathway

Abstract Human chorionic gonadotropin (hCG) is a luteotropic hormone that promotes the survival and steroidogenic activity of corpus luteum (CL) by acting through luteinizing hormone receptors (LHRs) expressed on luteinized theca and granulosa cells (GCs). Therefore, it is used to support luteal phase in in vitro fertilization (IVF) cycles to improve clinical pregnancy rates and prevent miscarriage. However, the molecular mechanism underlying this action of hCG is not well characterized. To address this question, we designed an in vitro translational research study on the luteal GCs obtained from 58 IVF patients. hCG treatment at different concentrations and time points activated c-Jun N-terminal kinase (JNK) pathway and significantly increased its endogenous kinase activity along with upregulated expression of steroidogenic enzymes (steroidogenic acute regulatory protein (stAR), 3β-Hydroxysteroid dehydrogenase (3β-HSD)) in a dose-dependent manner in the luteal GCs. As a result, in vitro P production of the cells was significantly enhanced after hCG. When JNK pathway was inhibited pharmacologically or knocked-down with small interfering RNA luteal function was compromised, P4 production was declined along with the expression of stAR and 3β-HSD in the cells. Further, hCG treatment after JNK inhibition failed to correct the luteal defect and promote P4 output. Similar to hCG, luteinizing hormone (LH) treatment improved luteal function as well and this action of LH was associated with JNK activation in the luteal GCs. These findings could be important from the perspective of CL biology and luteal phase in human because we for the first time identify a critical role for JNK signaling pathway downstream LHR activation by hCG/LH in luteal GCs. Summary Sentence JNK signaling pathway plays a central role in the upregulated expression of the steroidogenic enzymes StAR and 3b-HSD and augmented progesterone production by hCG/LH in human luteal granulosa cells.

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

Cell Death and Disease ◽

10.1038/cddis.2016.138 ◽

2016 ◽

Vol 7 (6) ◽

pp. e2247-e2247 ◽

Cited By ~ 75

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

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

Biomedicine & Pharmacotherapy ◽

10.1016/j.biopha.2013.02.006 ◽

2013 ◽

Vol 67 (4) ◽

pp. 337-345 ◽

Cited By ~ 10

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

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Cis‐urocanic acid inhibits SAPK/JNK signaling pathway in UV‐B exposed human corneal epithelial cells in vitro

Acta Ophthalmologica ◽

10.1111/j.1755-3768.2011.3135.x ◽

2011 ◽

Vol 89 (s248) ◽

pp. 0-0

Author(s):

T PAIMELA ◽

HM JAUHONEN ◽

A KAUPPINEN ◽

JK LAIHIA ◽

L LEINO ◽

...

Keyword(s):

Epithelial Cells ◽

Signaling Pathway ◽

Urocanic Acid ◽

Corneal Epithelial Cells ◽

Jnk Signaling ◽

Corneal Epithelial ◽

Human Corneal Epithelial Cells ◽

Jnk Signaling Pathway

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

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00055.2019 ◽

2019 ◽

Vol 317 (5) ◽

pp. G670-G681 ◽

Cited By ~ 6

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.

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