Increased expression of YAP is associated with decreased cell autophagy in the eutopic endometrial stromal cells of endometriosis

Pei, Tianjiao; Huang, Xin; Long, Ying; Duan, Chang-Ling; Liu, Tingting; Li, Yujing; Huang, Wei

doi:10.1016/j.mce.2019.04.012

Cited by 24 publications

(20 citation statements)

References 42 publications

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“…seRNA UCA1-activated Hippo-YAP is associated with not only apoptosis, but also autophagy. Increased Hippo-YAP activation has been found to control autophagy, which involves in mammalian target of rapamycin (mTOR) pathway that is a notable regulator of autophagy [107]. A study on breast carcinoma MCF-7 cells confirmed that scutellarin treatment upregulates p-YAP and downregulates YAP levels, which represses cancer development via inducing autophagy [79].…”

Section: Serna Participates In Autophagy Regulationmentioning

confidence: 99%

Oncogenic seRNA functional activation: a novel mechanism of tumorigenesis

Tan

Tang

2020

Mol Cancer

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seRNA is a noncoding RNA (ncRNA) transcribed from active super-enhancer (SE), through which SE exerts biological functions and participates in various physiological and pathological processes. seRNA recruits cofactor, RNA polymerase II and mediator to constitute and stabilize chromatin loop SE and promoter region, which regulates target genes transcription. In tumorigenesis, DNA insertion, deletion, translocation, focal amplification and carcinogen factor mediate oncogenic SE generation, meanwhile, oncogenic SE transcribes into tumor-related seRNA, termed as oncogenic seRNA. Oncogenic seRNA participates in tumorigenesis through activating various signal-pathways. The recent reports showed that oncogenic seRNA implicates in a widespread range of cytopathological processes in cancer progression including cell proliferation, apoptosis, autophagy, epithelial-mesenchymal transition, extracellular matrix stiffness and angiogenesis. In this article, we comprehensively summarized seRNA's characteristics and functions, and emphatically introduced inducible formation of oncogenic seRNA and its functional mechanisms. Lastly, some research strategies on oncogenic seRNA were introduced, and the perspectives on cancer therapy that targets oncogenic seRNA were also discussed.

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Section: Serna Participates In Autophagy Regulationmentioning

confidence: 99%

Oncogenic seRNA functional activation: a novel mechanism of tumorigenesis

Tan

Tang

2020

Mol Cancer

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“…However, the role of autophagy in EM is controversial, thus whether autophagy in EM is beneficial or detrimental remains to be elucidated. Several studies have demonstrated that the expression levels of autophagy-related genes (for example, Beclin-1 and LC3-II) are markedly decreased and autophagy activation is downregulated in endometrial stromal cells of patients with EM compared with healthy controls (45)(46)(47). Functionally, autophagy inhibition contributes to endometrial cell invasion, whereas autophagy activation represses ESC proliferation, colony formation and invasion (48).…”

Section: Discussionmentioning

confidence: 99%

miR‑143‑3p inhibits endometriotic stromal cell proliferation and invasion by inactivating autophagy in endometriosis

Yang

Hang

et al. 2021

Mol Med Rep

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Endometriosis (EM) is a multifactorial and debilitating chronic benign gynecological disease, but the pathogenesis of the disease is not completely understood. Dysregulated expression of microRNAs (miRNA/miR) is associated with the etiology of EM due to their role in regulating endometrial stromal cell proliferation and invasion. The present study aimed to identify the functions and mechanisms underlying miR-143-3p in EM. To explore the role of miR-143-3p in EM, functional miRNAs were analyzed via bioinformatics analysis. miR-143-3p expression levels in endometriotic stromal cells (ESCs) and normal endometrial stromal cells (NESCs) were measured via reverse transcription-quantitative PCR. The role of miR-143-3p in regulating ESC proliferation and invasion was assessed by performing Cell Counting Kit-8 and Transwell assays, respectively. miR-143-3p expression was significantly upregulated in ESCs compared with NESCs. Functionally, miR-143-3p overexpression inhibited ESC proliferation and invasion, whereas miR-143-3p knockdown promoted ESC proliferation and invasion. Moreover, miR-143-3p inhibited autophagy activation in ESCs, as indicated by decreased green puncta, which represented autophagic vacuoles, decreased microtubule associated protein 1 light chain 3α expression and increased p62 expression in the miR-143-4p mimic group compared with the control group. Moreover, compared with the control group, miR-143-3p overexpression significantly decreased the expression levels of autophagy-related 2B (ATG2B), a newly identified target gene of miR-143-3p, in ESCs. ATG2B overexpression reversed miR-143-3p overexpression-mediated inhibition of ESC proliferation and invasion. Collectively, the results of the present study suggested that miR-143-3p inhibited EM progression, thus providing a novel target for the development of therapeutic agents against EM.

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“…Endometriotic stromal cells have an abnormal response to progesterone, which suppresses PTEN expression, suppresses autophagy, and reduces apoptosis in the menstrual cycle via the AKT/mTOR pathway 207 . Increased expression of YAP significantly decreased autophagy through the mTOR pathway in eutopic endometrium stromal cells 208 . Mullerian‐inhibiting substance (MIS) induced autophagy and apoptotic cell death and inhibited proliferation in vitro 104 .…”

Section: Potential New Pharmaceuticals and Their Target‐signaling Pathwaysmentioning

confidence: 99%

Pharmaceuticals targeting signaling pathways of endometriosis as potential new medical treatment: A review

Hung

Zhang

Tan

et al. 2021

Medicinal Research Reviews

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Endometriosis (EM) is defined as endometrial tissues found outside the uterus. Growth and development of endometriotic cells in ectopic sites can be promoted via multiple pathways, including MAPK/MEK/ERK, PI3K/Akt/mTOR, NF‐κB, Rho/ROCK, reactive oxidative stress, tumor necrosis factor, transforming growth factor‐β, Wnt/β‐catenin, vascular endothelial growth factor, estrogen, and cytokines. The underlying pathophysiological mechanisms include proliferation, apoptosis, autophagy, migration, invasion, fibrosis, angiogenesis, oxidative stress, inflammation, and immune escape. Current medical treatments for EM are mainly hormonal and symptomatic, and thus the development of new, effective, and safe pharmaceuticals targeting specific molecular and signaling pathways is needed. Here, we systematically reviewed the literature focused on pharmaceuticals that specifically target the molecular and signaling pathways involved in the pathophysiology of EM. Potential drug targets, their upstream and downstream molecules with key aberrant signaling, and the regulatory mechanisms promoting the growth and development of endometriotic cells and tissues were discussed. Hormonal pharmaceuticals, including melatonin, exerts proapoptotic via regulating matrix metallopeptidase activity while nonhormonal pharmaceutical sorafenib exerts antiproliferative effect via MAPK/ERK pathway and antiangiogenesis activity via VEGF/VEGFR pathway. N‐acetyl cysteine, curcumin, and ginsenoside exert antioxidant and anti‐inflammatory effects via radical scavenging activity. Natural products have high efficacy with minimal side effects; for example, resveratrol and epigallocatechin gallate have multiple targets and provide synergistic efficacy to resolve the complexity of the pathophysiology of EM, showing promising efficacy in treating EM. Although new medical treatments are currently being developed, more detailed pharmacological studies and large sample size clinical trials are needed to confirm the efficacy and safety of these treatments in the near future.

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Increased expression of YAP is associated with decreased cell autophagy in the eutopic endometrial stromal cells of endometriosis

Cited by 24 publications

References 42 publications

Oncogenic seRNA functional activation: a novel mechanism of tumorigenesis

Oncogenic seRNA functional activation: a novel mechanism of tumorigenesis

miR‑143‑3p inhibits endometriotic stromal cell proliferation and invasion by inactivating autophagy in endometriosis

Pharmaceuticals targeting signaling pathways of endometriosis as potential new medical treatment: A review

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