Inhibin subunit beta A promotes cell proliferation and metastasis of breast cancer through Wnt/β-catenin signaling pathway

Xueqin, Tao; Mei, Jinhong; Yuping, Huang

doi:10.1080/21655979.2021.1971028

Cited by 12 publications

(10 citation statements)

References 25 publications

(14 reference statements)

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“…A number of signaling pathways control abnormal EMT and cell proliferation, including the Wnt/β-catenin, MAPK and NF-κB signaling pathways (57)(58)(59). The MAPK pathway regulates physiological processes and pathologies, such as cell proliferation, apoptosis, inflammation, cell motility, differentiation and tumorigenesis (60,61).…”

Section: Discussionmentioning

confidence: 99%

Hesperidin inhibits tobacco smoke‑induced pulmonary cell proliferation and EMT in mouse lung tissues via the p38 signaling pathway

Liang

Zhang

et al. 2022

Oncol Lett

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Tobacco smoke (TS) is the major cause of lung cancer. The abnormal proliferation and epithelial-mesenchymal transition (EMT) of lung cells promote occurrence and development of lung cancer. The p38 pathway intervenes in this cancer development. Hesperidin also serves a role in human health and disease prevention. The roles of p38 in TS-mediated abnormal cell proliferation and EMT, and the hesperidin intervention thereof are not yet understood. In the present study, it was demonstrated that TS upregulated proliferating cell nuclear antigen, vimentin and N-cadherin expression, whereas it downregulated E-cadherin expression, as assessed using western blotting and reverse transcription-quantitative PCR. Furthermore, it was observed that inhibition of the p38 pathway inhibit TS-induced proliferation and EMT. Hesperidin treatment prevented the TS-induced activation of the p38 pathway, EMT and cell proliferation in mouse lungs. The findings of the present study may provide insights into the pathogenesis of TS-related lung cancer.

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Section: Discussionmentioning

confidence: 99%

Hesperidin inhibits tobacco smoke‑induced pulmonary cell proliferation and EMT in mouse lung tissues via the p38 signaling pathway

Liang

Zhang

et al. 2022

Oncol Lett

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“…Also linked to cellular proliferation, migration and invasion in other physiologies, inhibin beta A (also known as INHBA) was originally recognized as a subunit for the closely related activin and inhibin glycoproteins, which exert opposing functional effects. However, INHBA perturbation alone has been associated with aggressive tumor behavior, including acceleration of cell proliferation, epithelial mesenchymal transition (EMT), migration and invasion (78)(79)(80). Noteworthy, INHBA has been detected in the human endometrium and endometrial pathologies (81, 82); however, the role of INHBA in the endometrial stromal cell remains an open question.…”

Section: Transcriptomic Analyses Of T-hescs Depleted Of Src-3 Prior T...mentioning

confidence: 99%

Decidualization of human endometrial stromal cells requires steroid receptor coactivator-3

Maurya

Szwarc

Lonard

et al. 2022

Front. Reprod. Health

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Steroid receptor coactivator-3 (SRC-3; also known as NCOA3 or AIB1) is a member of the multifunctional p160/SRC family of coactivators, which also includes SRC-1 and SRC-2. Clinical and cell-based studies as well as investigations on mice have demonstrated pivotal roles for each SRC in numerous physiological and pathophysiological contexts, underscoring their functional pleiotropy. We previously demonstrated the critical involvement of SRC-2 in murine embryo implantation as well as in human endometrial stromal cell (HESC) decidualization, a cellular transformation process required for trophoblast invasion and ultimately placentation. We show here that, like SRC-2, SRC-3 is expressed in the epithelial and stromal cellular compartments of the human endometrium during the proliferative and secretory phase of the menstrual cycle as well as in cultured HESCs. We also found that SRC-3 depletion in cultured HESCs results in a significant attenuation in the induction of a wide-range of established biomarkers of decidualization, despite exposure of these cells to a deciduogenic stimulus and normal progesterone receptor expression. These molecular findings are supported at the cellular level by the inability of HESCs to morphologically transform from a stromal fibroblastoid cell to an epithelioid decidual cell when endogenous SRC-3 levels are markedly reduced. To identify genes, signaling pathways and networks that are controlled by SRC-3 and potentially important for hormone-dependent decidualization, we performed RNA-sequencing on HESCs in which SRC-3 levels were significantly reduced at the time of administering the deciduogenic stimulus. Comparing HESC controls with HESCs deficient in SRC-3, gene enrichment analysis of the differentially expressed gene set revealed an overrepresentation of genes involved in chromatin remodeling, cell proliferation/motility, and programmed cell death. These predictive bioanalytic results were confirmed by the demonstration that SRC-3 is required for the expansion, migratory and invasive activities of the HESC population, cellular properties that are required in vivo in the formation or functioning of the decidua. Collectively, our results support SRC-3 as an important coregulator in HESC decidualization. Since perturbation of normal homeostatic levels of SRC-3 is linked with common gynecological disorders diagnosed in reproductive age women, this endometrial coregulator—along with its new molecular targets described here—may open novel clinical avenues in the diagnosis and/or treatment of a non-receptive endometrium, particularly in patients presenting non-aneuploid early pregnancy loss.

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“…As a highly conserved pathway, the Wnt/β-catenin pathway is widely involved in a number of malignant events, such as cell proliferation, cell apoptosis, vasculogenesis and metastasis [ 29 , 30 , 31 , 32 ]. In general, β-catenin is located in the cytoplasm and degraded by the destruction complex, which consists of Axin, adenomatosis polyposis coli (APC), glycogen synthase kinase 3β (GSK-3β), protein phosphatase 2A (PP2A), and casein kinase 1α (CK1α) in the absence of Wnt ligand.…”

Section: Functions and Mechanisms Of Ncrna-encoded Peptides/proteins ...mentioning

confidence: 99%

A Whole New Comprehension about ncRNA-Encoded Peptides/Proteins in Cancers

Chen

Shen²,

Nie³

et al. 2022

Cancers

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It is generally considered that non-coding RNAs do not encode proteins; however, more recently, studies have shown that lncRNAs and circRNAs have ORFs which are regions that code for peptides/protein. On account of the lack of 5’cap structure, translation of circRNAs is driven by IRESs, m6A modification or through rolling amplification. An increasing body of evidence have revealed different functions and mechanisms of ncRNA-encoded peptides/proteins in cancers, including regulation of signal transduction (Wnt/β-catenin signaling, AKT-related signaling, MAPK signaling and other signaling), cellular metabolism (Glucose metabolism and Lipid metabolism), protein stability, transcriptional regulation, posttranscriptional regulation (regulation of RNA stability, mRNA splicing and translation initiation). In addition, we conclude the existing detection technologies and the potential of clinical applications in cancer therapy.

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Inhibin subunit beta A promotes cell proliferation and metastasis of breast cancer through Wnt/β-catenin signaling pathway

Cited by 12 publications

References 25 publications

Hesperidin inhibits tobacco smoke‑induced pulmonary cell proliferation and EMT in mouse lung tissues via the p38 signaling pathway

Hesperidin inhibits tobacco smoke‑induced pulmonary cell proliferation and EMT in mouse lung tissues via the p38 signaling pathway

Decidualization of human endometrial stromal cells requires steroid receptor coactivator-3

A Whole New Comprehension about ncRNA-Encoded Peptides/Proteins in Cancers

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