Abscisic Acid-Induced Autophagy Selectively via MAPK/JNK Signalling Pathway in Glioblastoma

Zhou, Nan; Wei, Zixuan; Qi, Zengxin; Chen, Liang

doi:10.1007/s10571-020-00888-1

Cited by 19 publications

(9 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this setting, aggressive cancers can be addicted to autophagy for survival. Multiple signaling pathways are involved in the process of autophagy, such as mitogen-activated protein kinases (MAPK)/JNK, phosphatidylinositol-3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR), and PKC-related signaling pathway [ 54 , 55 , 56 ]. PKC enzymes contribute to cellular homeostasis maintenance by regulating the autophagy of cellular components.…”

Section: Pkcs In Cancermentioning

confidence: 99%

Targeting Protein Kinase C for Cancer Therapy

Huang

et al. 2022

Cancers

View full text Add to dashboard Cite

Protein kinase C (PKC) isoforms, a group of serine-threonine kinases, are important regulators in carcinogenesis. Numerous studies have demonstrated that PKC isoforms exert both positive and negative effects on cancer cell demise. In this review, we systematically summarize the current findings on the architecture, activity regulation and biological functions of PKCs, especially their relationship with anti-cancer therapy-induced cell death. Additionally, we elaborate on current knowledge of the effects of PKCs on tumor metabolism and microenvironment, which have gained increasing attention in oncology-related areas. Furthermore, we underscore the basic experimental and clinical implications of PKCs as a target for cancer therapy to evaluate their therapeutic benefits and potential applications.

show abstract

Section: Pkcs In Cancermentioning

confidence: 99%

Targeting Protein Kinase C for Cancer Therapy

Huang

et al. 2022

Cancers

View full text Add to dashboard Cite

show abstract

“…In recent years, many natural extracts have been reported to affect the progression of malignant tumors through autophagy. For example, as a plant hormone, abscisic acid can induce autophagy in glioma cells through the MAPK/JNK signaling pathway [ 21 ], and the lectin of Dioclea violacea induces autophagy and causes the death of glioma cell U87MG [ 22 ]. Autophagy can be used as a new target for the treatment of tumors and even gliomas.…”

Section: Introductionmentioning

confidence: 99%

Arctigenin Inhibits Glioblastoma Proliferation through the AKT/mTOR Pathway and Induces Autophagy

Jiang

Liu

Wangwang

et al. 2020

BioMed Research International

View full text Add to dashboard Cite

Purpose. Arctigenin (ARG) is a natural lignan compound extracted from Arctium lappa and has displayed anticancer function and therapeutic effect in a variety of cancers. Arctigenin is mainly from Arctium lappa extract. It has been shown to induce autophagy in various cancers. However, as for whether arctigenin induces autophagy in gliomas or not, the specific mechanism is still worth exploring. Methods. Using CCK8, the monoclonal experiment was made to detect the proliferation ability. The scratch experiment and the transwell experiment were applied to the migration and invasion ability. PI/RNase and FITC-conjugated anti-annexin V were used to detect the cell cycle and apoptosis. Western blotting was used to determine the specified protein level, and constructed LC3B-GFP plasmid was used for analysis of autophagy.Results. Our research showed that ARG inhibited the growth and proliferation and invasion and migration of glioma cells in a dose-dependent manner (U87MG and T98G) and arrested the cell cycle and induced apoptosis. Interestingly, ARG induced autophagy in a dose-dependent manner. We applied Western blotting to measure the increase in the key autophagy protein LC3B, as well as some other autophagy-related proteins (increase in Beclin-1 and decrease in P62). In order to further explore the mechanism that ARG passed initiating autophagy to inhibit cell growth, we further found by Western blotting that AKT and mTOR phosphorylation proteins (P-AKT, P-mTOR) were reduced after ARG treatment, and we used AKT agonists to rescue, and the phosphorylated proteins of AKT and mTOR increased, and we found that the autophagy-related proteins were also reversed. And interestingly, the protein of apoptosis was also reversed along with autophagy. Conclusions. We thought ARG inhibited the proliferation of glioma cells by inducing autophagy and apoptosis through the AKT/mTOR pathway.

show abstract

“…As a negative regulator of MAPK, DUSP4 can inhibit JNK signaling [2,16]. JNK is widely considered to be a pro-autophagic molecule, which results into autophagic cell death of tumors [21][22][23]. JNK-Beclin1-autophagy signaling is a classic pathway of JNKregulated autophagy activation [17,24,25].…”

Section: Discussionmentioning

confidence: 99%

“…JNK can also promote cell death by activating autophagy, which is re ected in some malignant tumours [21][22][23]. Activated JNK is known to dissociate the autophagy molecule Beclin1 from BCL2-Beclin1 complex, and free Beclin1 can activate autophagy after entering autophagy ux [17].…”

Section: Introductionmentioning

confidence: 99%

TAT-Beclin1 Represses the Carcinogenesis of DUSP4-positive PTC by Enhancing Autophagy

Zang

Song

Tian

et al. 2021

Preprint

View full text Add to dashboard Cite

Background: DUSP4 is a pro-tumorigenic molecule of papillary thyroid carcinoma (PTC). DUSP4 also exists as an autophagic regulator. Moreover, DUSP4, as a negative regulator of MAPK, can prevent Beclin1 from participating in autophagic response. This study aimed to explore whether TAT-Beclin1, a recombinant protein of Beclin1, could inhibit the tumorigenesis of DUSP4-positive PTC by regulating autophagy.Methods: First, we divided PTC cancer tissues into three groups according to DUSP4 expression levels by immunohistochemical analyses, and evaluated the relationship between the expression of autophagic proteins (Beclin1 and LC3II) and DUSP4 expression using Western blotting assays. After overexpression of DUSP4 by lentiviral transduction, the roles of TAT-Beclin1 on DUSP4-overexpressed PTC was detected.Results: Our results showed that the expression levels of autophagic proteins (Beclin1 and LC3II) increased with the increase of DUSP4 expression in PTC carcinomas. In PTC cells, DUSP4 overexpression-inhibited autophagic activity (including Beclin1 expression, LC3 conversion rate and LC3-puncta formation) and -promoted cell proliferation and migration were reversed by TAT-Beclin1 administration. In vivo assays also showed that DUSP4-overexpressed PTC cells had stronger tumorigenic ability and weaker autophagic activity, which was recovered by TAT-Beclin1 administration. Conclusions: TAT-Beclin1, as an autophagic promoter, could repress the carcinogenesis of DUSP4-positive PTC, which implies that the addition of TAT-Beclin1 may be determined through detecting the levels of DUSP4 in the treatment of PTC.

show abstract

Abscisic Acid-Induced Autophagy Selectively via MAPK/JNK Signalling Pathway in Glioblastoma

Cited by 19 publications

References 38 publications

Targeting Protein Kinase C for Cancer Therapy

Targeting Protein Kinase C for Cancer Therapy

Arctigenin Inhibits Glioblastoma Proliferation through the AKT/mTOR Pathway and Induces Autophagy

TAT-Beclin1 Represses the Carcinogenesis of DUSP4-positive PTC by Enhancing Autophagy

Contact Info

Product

Resources

About