<scp>PLC</scp>γ2 promotes apoptosis while inhibits proliferation in rat hepatocytes through <scp>PKCD</scp>/<scp>JNK MAPK</scp> and <scp>PKCD</scp>/p38 <scp>MAPK</scp> signalling

Chen, Xiaoguang; Lv, Qiongxia; Ma, Jun; Liu, Yumei

doi:10.1111/cpr.12437

Cited by 13 publications

(7 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The JNK signalling pathway is tightly regulated and is implicated in a plethora of cellular function . However, the molecular mechanism that modulates the JNK signalling pathway remains elusive.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

FER promotes cell migration via regulating JNK activity

et al. 2019

Cell Proliferation

View full text Add to dashboard Cite

Objectives Cell migration has a key role in cancer metastasis, which contributes to drug resistance and tumour recurrence. Better understanding of the mechanisms involved in this process will potentially reveal new drug targets for cancer therapy. Fer is a non‐receptor protein tyrosine kinase aberrantly expressed in various human cancers, whereas its role in tumour progression remains elusive. Materials and Methods Transgenic flies and epigenetic analysis were employed to investigate the role of Drosophila Fer (FER) in cell migration and underlying mechanisms. Co‐immunoprecipitation assay was used to monitor the interaction between FER and Drosophila JNK (Bsk). The conservation of Fer in regulating JNK signalling was explored in mammalian cancer and non‐cancer cells. Results Overexpression of FER triggered cell migration and activated JNK signalling in the Drosophila wing disc. Upregulation and downregulation in the basal activity of Bsk exacerbated and eliminated FER‐mediated migration, respectively. In addition, loss of FER blocked signal transduction of the JNK pathway. Specifically, FER interacted with and promoted the activity of Bsk, which required both the kinase domain and the C‐terminal of Bsk. Lastly, Fer regulated JNK activities in mammalian cells. Conclusions Our study reveals FER as a positive regulator of JNK‐mediated cell migration and suggests its potential role as a therapeutic target for cancer metastasis.

show abstract

Section: Discussionmentioning

confidence: 99%

“…The JNK signalling pathway is tightly regulated and is implicated in a plethora of cellular function. 45,46 However, the molecular mechanism that modulates the JNK signalling pathway remains elusive. Here, we reported that FER was able to positively regulate JNK signalling, which was supported by several lines of evidence.…”

Section: Discussionmentioning

confidence: 99%

FER promotes cell migration via regulating JNK activity

et al. 2019

Cell Proliferation

View full text Add to dashboard Cite

show abstract

“…In combination with various databases and preliminary screening results, we selected three typical mRNAs for further verification. For example, PLCG2 could promote proliferation through inactivating ERK and NF-κB pathway ( Ma et al, 2019 ), p38 MAPK and JNK MAPK pathways ( Chen et al, 2018a ), PKCδ-mediated JNK1/2 signaling pathway ( Chen et al, 2018b ). The TPR contributes to the organization of the nuclear lamina and in cooperation with lamins guards the interphase assembly of nuclear pore complexes ( Fišerová et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

Analysis of N6-Methyladenosine Methylome in Adenocarcinoma of Esophagogastric Junction

Huang

et al. 2022

Front. Genet.

View full text Add to dashboard Cite

Background: From previous studies, we found that there are more than 100 types of RNA modifications in RNA molecules. m6A methylation is the most common. The incidence rate of adenocarcinoma of the esophagogastric junction (AEG) at home and abroad has increased faster than that of stomach cancer at other sites in recent years. Here, we systematically analyze the modification pattern of m6A mRNA in adenocarcinoma at the esophagogastric junction.Methods: m6A sequencing, RNA sequencing, and bioinformatics analysis were used to describe the m6A modification pattern in adenocarcinoma and normal tissues at the esophagogastric junction.Results: In AEG samples, a total of 4,775 new m6A peaks appeared, and 3,054 peaks disappeared. The unique m6A-related genes in AEG are related to cancer-related pathways. There are hypermethylated or hypomethylated m6A peaks in AEG in differentially expressed mRNA transcripts.Conclusion: This study preliminarily constructed the first m6A full transcriptome map of human AEG. This has a guiding role in revealing the mechanism of m6A-mediated gene expression regulation.

show abstract

“…MAPK is a class of serine/threonine-protein kinases, including three main types of subfamily members: the extracellular-signal-regulated kinases (ERKs), the c-jun N-terminal kinase (JNKs), and the p38 kinases ( Lee et al, 2020 ; Sinkala et al, 2021 ). They can transfer the extracellular signals into the nucleus via the MAP3K–MAP2K–MAPK cascade to participate in cellular activities like proliferation, differentiation, and apoptosis ( Chen et al, 2018 ; Ostojic et al, 2021 ). It was reported that bone marrow stem cell-derived extracellular vesicles (BMSC-EVs) could alleviate the IL-1β-induced chondrocyte inflammatory phenotype ( Zhang B et al, 2022 ), and such effect was further improved with the treatment of BMSC-EV generated in a hypoxic environment.…”

Section: Mir-17-92 In Cartilage Degradationmentioning

confidence: 99%

miR-17-92 cluster in osteoarthritis: Regulatory roles and clinical utility

et al. 2022

View full text Add to dashboard Cite

Osteoarthritis (OA) is the most prevalent articular disease, especially in aged population. Caused by multi-factors (e.g., trauma, inflammation, and overloading), OA leads to pain and disability in affected joints, which decreases patients’ quality of life and increases social burden. In pathophysiology, OA is mainly characterized by cartilage hypertrophy or defect, subchondral bone sclerosis, and synovitis. The homeostasis of cell–cell communication is disturbed as well in such pro-inflammatory microenvironment, which provides clues for the diagnosis and treatment of OA. MicoRNAs (miRNAs) are endogenous non-coding RNAs that regulate various processes via post-transcriptional mechanisms. The miR-17-92 cluster is an miRNA polycistron encoded by the host gene called MIR17HG. Mature miRNAs generated from MIR17HG participate in biological activities such as oncogenesis, neurogenesis, and modulation of the immune system. Accumulating evidence also indicates that the expression level of miRNAs in the miR-17-92 cluster is tightly related to the pathological processes of OA, such as chondrocyte apoptosis, extracellular matrix degradation, bone remodeling, and synovitis. In this review, we aim to summarize the roles of the miR-17-92 cluster in the underlying molecular mechanism during the development and progression of OA and shed light on the new avenue of the diagnosis and treatment of OA.

show abstract

PLCγ2 promotes apoptosis while inhibits proliferation in rat hepatocytes through PKCD/JNK MAPK and PKCD/p38 MAPK signalling

Abstract: This study showed that PLCγ2 regulates hepatocyte growth through PKCD-dependently activating p38 MAPK and JNK MAPK pathways; this result was experimentally based on the further exploration of the effect of PLCγ2 on hepatocyte growth in vivo.

Cited by 13 publications

References 37 publications

FER promotes cell migration via regulating JNK activity

FER promotes cell migration via regulating JNK activity

Analysis of N6-Methyladenosine Methylome in Adenocarcinoma of Esophagogastric Junction

miR-17-92 cluster in osteoarthritis: Regulatory roles and clinical utility

Contact Info

Product

Resources

About