Triple-negative and triple-positive breast cancer cells reciprocally control their growth and migration via the S100A4 pathway

Dukhanina, E. A.; Portseva, T. N.; Dukhanin, A. S.; Георгиева, С. Г.

doi:10.1080/19336918.2022.2072554

Cited by 3 publications

(2 citation statements)

References 17 publications

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“…Therefore, we performed experiments and found that S100A4 can promote the proliferation of endometrial epithelial cells. In a previous study, S100A4 protein was overexpressed in cultured cancer cells; the results showed that S100A4 protein overexpression did not significantly affect the proliferation of MCF-7 cells but inhibited the proliferation of MDA-MB-231 cells ( 44 ). Similarly, S100A4 was found to regulate cell migration but not cell proliferation in gastric adenocarcinoma ( 20 ).…”

Section: Discussionmentioning

confidence: 96%

GnRH-mediated suppression of S100A4 expression inhibits endometrial epithelial cell proliferation in sheep via GNAI2/MAPK signaling

Jiao,

Chu,

et al. 2024

Front. Vet. Sci.

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BackgroundGonadotrophin-releasing hormone (GnRH) administration significantly decreases the pregnancy rate of recipient ewes after embryo transfer, possibly because GnRH affects endometrial epithelial cell function. Therefore, this study investigated the effect of GnRH on endometrial epithelial cells.MethodsTranscriptome sequencing was used to determine the regulatory effect of GnRH on the ewe endometrium, and the S100A4 gene, which showed altered transcription, was screened as a candidate regulator of this effect. Endometrial epithelial cells were further isolated, the S100A4 protein was immunoprecipitated, and host proteins that interacted with S100A4 were identified by mass spectrometry. We further verified the effects of S100A4 and GNAI2 on the proliferation of endometrial epithelial cells via overexpression/knockdown experiments and subsequent CCK-8 and EdU assays. The effect of S100A4 deletion in endometrial cells on reproduction was verified in mice with S100A4 knockout.ResultsOur results showed that S100A4 gene transcription in endometrial cells was significantly inhibited after GnRH administration. GNAI2 was identified as a downstream interacting protein of S100A4, and S100A4 was confirmed to activate the MAPK signaling pathway to promote cell proliferation by targeting GNAI2.ConclusionGnRH can suppress the expression of S100A4 in the endometrium, consequently inhibiting the proliferation of endometrial cells through the S100A4/GNAI2/MAPK signaling pathway. These findings suggest a potential explanation for the limited efficacy of GnRH in promoting embryo implantation.

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Section: Discussionmentioning

confidence: 96%

GnRH-mediated suppression of S100A4 expression inhibits endometrial epithelial cell proliferation in sheep via GNAI2/MAPK signaling

Jiao,

Chu,

et al. 2024

Front. Vet. Sci.

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“…Breast cancer has much higher morbidity rate than other cancers, so people should take breast cancer seriously ( Ahmad, 2019 ). Triple-negative breast cancer (TNBC) is a subtype of breast cancer ( Dukhanina et al, 2022 ). The disease is characterized by high invasiveness, poor responsiveness to therapy, and difficulty with treatment ( Medina et al, 2020 ; Luna-Dulcey et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

WXJ-202, a novel Ribociclib derivative, exerts antitumor effects against breast cancer through CDK4/6

Ji¹,

Liu²,

Xu³

et al. 2023

Front. Pharmacol.

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Cyclin-dependent kinases 4 and 6 (CDK4/6) are key regulatory proteins in the cell division and proliferative cycle in humans. They are overactive in many malignant tumors, particularly in triple-negative breast cancer (TNBC). Inhibition of CDK4/6 targets can have anti-tumor effects. Here, we designed and synthesized a novel derivative of Ribociclib that could affect CDK4/6, named WXJ-202. This study aimed to investigate the effects of compound WXJ-202 on proliferation, apoptosis, and cell cycle arrest in human breast cancer cell lines and their molecular mechanisms. We assayed cell viability with methyl thiazolyl tetrazolium (MTT) assay. Clone formation, migration, and invasion ability were assayed by clone formation assay, wound healing assay, and transwell invasion assay. The effect of compound WXJ-202 on apoptosis and cell cycle was detected by flow cytometry analysis. Western blotting was performed to detect the expression of proteins related to the CDK4/6-Rb-E2F pathway. The anti-cancer effects were studied in vivo transplantation tumor models. WXJ-202 was shown to inhibit cell proliferation, colony formation, migration, and invasion, as well as induce apoptosis and cycle arrest in breast cancer cells. The levels of proteins related to the CDK4/6-Rb-E2F pathway, such as CDK4, CDK6, and p-Rb, were decreased. Finally, studies had shown that compound WXJ-202 exhibited significant anti-tumor activity in transplantation tumor models. In this research, the compound WXJ-202 was shown to have better anti-tumor cell proliferative effects and could be used as a potential candidate against TNBC tumors.

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S100A4 targets PPP1CA/IL-17 to inhibit the senescence of sheep endometrial epithelial cells

Jiao,

Cui

et al. 2024

Front. Vet. Sci.

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BackgroundGonadotropin-releasing hormone (GnRH) is commonly used in animal reproduction and production, but it was previously reported that GnRH decreases the embryo implantation rate during artificial insemination or embryo transfer in sheep. In addition to the finding that GnRH can target S100A4 to inhibit endometrial epithelial cells proliferation, it was also found that endometrial cells were in poor condition and experienced cell death in S100A4 knockout mice, but the mechanism is unclear.MethodsThe protein PPP1CA, which interacts with S100A4, was detected by immunoprecipitation-mass spectrometry of overexpression and knockdown of S100A4 and PPP1CA. The effect of S100A4 and PPP1CA on cell senescence was detected by Galactosidase staining. To further reveal the mechanism effect of S100A4 and PPP1CA on cell senescence, transcriptome sequencing was conducted. Additionally, in vivo experiments were performed to assess PPP1CA protein expression in the endometrial tissue of S100A4 knockout mice.ResultsS100A4 inhibited cell senescence by activating PPP1CA, while PPP1CA overexpression suppressed the activation of the IL-17 signaling pathway. Inhibition of the IL-17 signaling pathway inhibited the senescence of endometrial cells.ConclusionS100A4 can target the PPP1CA/IL-17 signaling pathway and inhibit endometrial epithelial cell senescence.

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Triple-negative and triple-positive breast cancer cells reciprocally control their growth and migration via the S100A4 pathway

Cited by 3 publications

References 17 publications

GnRH-mediated suppression of S100A4 expression inhibits endometrial epithelial cell proliferation in sheep via GNAI2/MAPK signaling

GnRH-mediated suppression of S100A4 expression inhibits endometrial epithelial cell proliferation in sheep via GNAI2/MAPK signaling

WXJ-202, a novel Ribociclib derivative, exerts antitumor effects against breast cancer through CDK4/6

S100A4 targets PPP1CA/IL-17 to inhibit the senescence of sheep endometrial epithelial cells

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