Talin1 Induces Epithelial-Mesenchymal Transition to Facilitate Endometrial Cell Migration and Invasion in Adenomyosis Under the Regulation of microRNA-145-5p

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Talin1 is overexpressed in adenomyosis, where it induces epithelial-mesenchymal transition, enhancing cell migration and invasion by activating the wnt/β-catenin pathway, and is negatively regulated by microRNA-145-5p.

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This study investigated the clinical expression and mechanistic role of Talin1, microRNA-145-5p (miR-145-5p), and epithelial-mesenchymal transition (EMT) markers in adenomyosis using qRT-PCR, immunohistochemistry/immunofluorescence, western blot for EMT and Wnt/β-catenin pathway proteins, and in vitro wound healing/transwell assays with adenomyosis eutopic and ectopic endometrial epithelial cells. Talin1 was markedly overexpressed while miR-145-5p was downregulated in ADS tissues and cells, and Talin1 overexpression induced EMT and increased migration and invasion by activating canonical Wnt/β-catenin signaling. Dual-luciferase reporter assays supported that miR-145-5p inversely regulates Talin1 as a direct target. The main limitation stated in the abstract is that the precise molecular mechanism of Talin1 in adenomyosis had been extremely scanty before, implying the work is mechanistic and largely in vitro without broader in vivo validation described here. This paper is centrally about adenomyosis — it tests how the miR-145-5p/Talin1 axis drives EMT and endometrial cell migration and invasion via Wnt/β-catenin signaling in adenomyosis.

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Abstract

Adenomyosis (ADS) is a commonly encountered benign gynecological disorder. Epithelial-mesenchymal transition (EMT) may serve a pivotal role in the pathogenesis of ADS. Talin1 has been identified to be implicated in multiple human carcinomas, probably through inducing EMT process. However, available data on the precise molecular mechanism of Talin1 in the pathogenesis of ADS remain extremely scanty. In the present study, we aim to investigate the clinical roles of Talin1 and its effects on uterine endometrial cell migration, invasion, and EMT in ADS. Relative mRNA expression of Talin1, microRNA-145-5p (miR-145-5p), and EMT-related markers was determined by qRT-PCR. Immunohistochemistry and immunofluorescence were performed to examine the distribution of Talin1 in ADS endometrium. Protein levels of Talin1, EMT-related markers, and wnt/β-catenin pathway were measured by western blot. Wound healing assay and transwell assay were utilized for evaluating cell migration and invasion respectively. Dual-luciferase reporter assay was performed to verify the relationship between Talin1 and miR-145-5p. We found Talin1 was markedly overexpressed in ADS endometrial tissue and cells, whereas miR-145-5p was downregulated. Elevated Talin1 mRNA level might be closely related to some clinicopathological features of ADS. Through functional experiments, we demonstrated that overexpression of Talin1 induced EMT and enhanced migration and invasion ability of ADS eutopic and ectopic endometrial epithelial cells (ADS_Eu_EEC and ADS_Ec_EEC) in vitro through activating the canonical wnt/β-catenin pathway. From a mechanistic perspective, Talin1 was inversely regulated by miR-145-5p as a direct target. Our findings unveiled that under the regulation of miR-145-5p, Talin1 might promote endometrial cell migration and invasion through inducing EMT, presenting a novel insight for elucidating the pathogenesis of ADS.
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Abstract

Adenomyosis (ADS) is a commonly encountered benign gynecological disorder. Epithelial-mesenchymal transition (EMT) may serve a pivotal role in the pathogenesis of ADS. Talin1 has been identified to be implicated in multiple human carcinomas, probably through inducing EMT process. However, available data on the precise molecular mechanism of Talin1 in the pathogenesis of ADS remain extremely scanty. In the present study, we aim to investigate the clinical roles of Talin1 and its effects on uterine endometrial cell migration, invasion, and EMT in ADS. Relative mRNA expression of Talin1, microRNA-145-5p (miR-145-5p), and EMT-related markers was determined by qRT-PCR. Immunohistochemistry and immunofluorescence were performed to examine the distribution of Talin1 in ADS endometrium. Protein levels of Talin1, EMT-related markers, and wnt/β-catenin pathway were measured by western blot. Wound healing assay and transwell assay were utilized for evaluating cell migration and invasion respectively. Dual-luciferase reporter assay was performed to verify the relationship between Talin1 and miR-145-5p. We found Talin1 was markedly overexpressed in ADS endometrial tissue and cells, whereas miR-145-5p was downregulated. Elevated Talin1 mRNA level might be closely related to some clinicopathological features of ADS. Through functional experiments, we demonstrated that overexpression of Talin1 induced EMT and enhanced migration and invasion ability of ADS eutopic and ectopic endometrial epithelial cells (ADS_Eu_EEC and ADS_Ec_EEC) in vitro through activating the canonical wnt/β-catenin pathway. From a mechanistic perspective, Talin1 was inversely regulated by miR-145-5p as a direct target. Our findings unveiled that under the regulation of miR-145-5p, Talin1 might promote endometrial cell migration and invasion through inducing EMT, presenting a novel insight for elucidating the pathogenesis of ADS. Similar content being viewed by others Data Availability The data used to support the findings of this study are available from the corresponding author upon request.

References

Shen X, Duan H, Wang S, et al. Decreased expression of cannabinoid receptors in the eutopic and ectopic endometrium of patients with adenomyosis [J]. Biomed Res Int. 2019;2019:5468954. Donnez J, Donnez O, Dolmans M-M. Introduction: Uterine adenomyosis, another enigmatic disease of our time [J]. Fertil Steril. 2018;109:369–70. Garcia-Solares J, Donnez J, Donnez O, Dolmans M-M. Pathogenesis of uterine adenomyosis: invagination or metaplasia? Fertil Steril. 2018;109(3):371–9. Guo S-W. The pathogenesis of adenomyosis vis-à-vis endometriosis.[J]. J Clin Med. 2020;9(2). https://doi.org/10.3390/jcm9020485. Benagiano G, Brosens I, Habiba M. Structural and molecular features of the endomyometrium in endometriosis and adenomyosis.[J]. Hum Reprod Update. 2014;20:386–402. Yen Chih F, Huang J, Lee Chyi L, et al. Molecular characteristics of the endometrium in uterine adenomyosis and its biochemical microenvironment [J]. Reprod Sci. 2017;24:1346–61. A. Puisieux, T. Brabletz, J. Caramel. Oncogenic roles of EMT-inducing transcription factors. [J] .Nat Cell Biol,2014,16(6):488–494. Brabletz T, Kalluri R, Nieto M-A, Weinberg R-A. EMT in cancer [J]. Nat Rev Cancer. 2018;18(2):128–34. Yang J, Weinberg R-A. Epithelial-mesenchymal transition: at the crossroads of development and tumor metastasis. [J]. Dev Cell. 2008;14:818–29. Chen Y-J, Li H-Y, Huang C-H, et al. Oestrogen-induced epithelial-mesenchymal transition of endometrial epithelial cells contributes to the development of adenomyosis.[J]. J Pathol. 2010;222:261–70. Oh S-J, Shin J-H, Kim T-H, et al. β-Catenin activation contributes to the pathogenesis of adenomyosis through epithelial-mesenchymal transition.[J]. J Pathol. 2013;231:210–22. Liu X-S, Shen M-H, Q-M, Qi S-W. Corroborating evidence for platelet-induced epithelial-mesenchymal transition and fibroblast-to-myofibroblast transdifferentiation in the development of adenomyosis.[J]. Hum Reprod. 2016;31:734–49. Gough RE, Goult BT. The tale of two talins - two isoforms to fine-tune integrin signalling. [J]. FEBS Lett. 2018;592:2108–25. Ji L, Jiang F-Z, Cui W-P, Ji C-KQ. Talin1 knockdown prohibits the proliferation and migration of colorectal cancer cells via the EMT signaling pathway.[J]. Oncol Lett. 2019;18:5408–16. Jiang J-F, Sun A-J, Wang Y-F, Deng Y. Increased expression of Talin1 in the eutopic and ectopic endometria of women with adenomyosis.[J]. Gynecol Endocrinol. 2016;32:469–72. Shen X, Duan H, Wang S, Wang Y-Y, Lin S-L. Expression of cannabinoid receptors in myometrium and its correlation with dysmenorrhea in adenomyosis.[J]. Reprod Sci. 2019;26:1618–25. Lin S-L, Duan H, Wang S, Li J-J. Overexpression of Lin28B promoted the proliferation of adenomyotic smooth muscle cells of the junctional zone via regulating Let-7a.[J]. Reprod Sci. 2020;27:1156–63. Zuo W-W, Wu X-Y, Liu H-O, et al. P21-activated kinase 1 overactivates in eutopic endometrium of adenomyosis.[J]. Reprod Sci. 2019;26(9):1235–42. Chen S-J, Xu J-Y, Su Y, et al. MicroRNA-145 suppresses epithelial to mesenchymal transition in pancreatic cancer cells by inhibiting TGF-β signaling pathway.[J]. J Cancer. 2020;11(9):2716–23. Jiang S-B, He X-J, Xia Y-J, et al. MicroRNA-145-5p inhibits gastric cancer invasiveness through targeting N-cadherin and ZEB2 to suppress epithelial-mesenchymal transition.[J]. Onco Targets Ther. 2016;9:2305–15. Leyendecke G, Bilgicyildirim A, Inacker M, Stalf T, Huppert P, et al. Adenomyosis and endometriosis. Re-visiting their association and further insights into the mechanisms of auto-traumatisation. An MRI study.[J]. Arch Gynecol Obstet. 2015;291:917–32. Leyendecker G, Wildt L. A new concept of endometriosis and adenomyosis: tissue injury and repair (TIAR).[J]. Horm Mol Biol Clin Invest. 2011;5:125–42. Shen M, Liu Z, Zhang H, Guo S-W. Transforming growth factor β1 signaling coincides with epithelial-mesenchymal transition and fibroblast-to-myofibroblast transdifferentiation in the development of adenomyosis in mice.[J]. Hum Reprod. 2016;31:355–69. Thiery JP, Acloque H, Huang RY, Nieto MA. Epithelial-mesenchymal transitions in development and disease. Cell. 2009;139(5):871–90. Vannuccini S, Tosti C, Carmona F, et al. Petraglia. Pathogenesis of adenomyosis: an update on molecular mechanisms.[J]. Reprod BioMed Online. 2017;35:592–601. Malla R-R, Vempati R-K. Talin: a potential drug target for cancer therapy.[J]. Curr Drug Metab. 2020;21(1):25–32. Kopp PM, Bate N, Hansen TM, et al. Studies on the morphology and spreading of human endothelial cells define key inter- and intramolecular interactions for talin1.[J]. Eur J Cell Biol. 2010;89:661–73. Halder A, Nayak KB, Chakraborty S. Ecotopic viral integration site 1 (EVI1) transcriptionally targets talin1 (TLN1) and upregulates its expression in chronic myeloid leukemia.[J]. Leuk Lymphoma. 2018;59:2008–10. Malla RR, Vempati RK. Talin: a potential drug target for cancer therapy.[J]. Curr Drug Metab. 2020;21:25–32. Haydari Z, Shams H, Jahed Z, et al. Kindlin assists Talin to promote integrin activation.[J]. Biophys J. 2020;118(8):1977–91. Rosemarie EG, Benjamin TG. The tale of two talins - two isoforms to fine-tune integrin signalling.[J]. FEBS Lett. 2018;592:2108–25. Shen Y, Qin A-P. Regulation of embryonic signal on Talin1 in mouse endometrium.[J]. Reprod Sci. 2019;26:1277–86. Ji L, Jiang FZ, Cui XP, Qin CK. Talin1 knockdown prohibits the proliferation and migration of colorectal cancer cells via the EMT signaling pathway. Oncol Lett. 2019;18(5):5408–16. Lacheta J. Uterine adenomyosis: pathogenesis, diagnostics, symptomatology and treatment.[J]. Ceska Gynekol. 2019;84:240–6. Munro Malcolm G. Uterine polyps, adenomyosis, leiomyomas, and endometrial receptivity.[J]. Fertil Steril. 2019;111:629–40. Mehasseb MK, Panchal R, Taylor AH, Brown L, et al. Estrogen and progesterone receptor isoform distribution through the menstrual cycle in uteri with and without adenomyosis.[J]. Fertil Steril. 2011;95:2228–35 2235.e1. Li J-J, Chung Jacqueline PW, Wang S, Li TC, Duan H. The investigation and management of adenomyosis in women who wish to improve or preserve fertility.[J]. Biomed Res Int. 2018;2018:6832685. Polyak K, Weinber RA. Transitions between epithelial and mesenchymal states: acquisition of malignant and stem cell traits.[J]. Nat Rev Cancer. 2009;9:265–73. He S-Y, Huang Y-F, Dong S-Q, et al. MiR-199a-3p/5p participated in TGF-β and EGF induced EMT by targeting DUSP5/MAP3K11 in pterygium.[J]. J Transl Med. 2020;18:332. Cao J, Liu D, Zhao S-Y, Yuan L-W, et al. Estrogen attenuates TGF-β1-induced EMT in intrauterine adhesion by activating Wnt/β-catenin signaling pathway.[J]. Braz J Med Biol Res. 2020;53:e9794. Pyo Min C, Chae Seung A, Yoo J-H, Lee K-W. A induces epithelial-to-mesenchymal transition and renal fibrosis through TGF-β/Smad2/3 and Wnt1/β-catenin signaling pathways in vitro and in vivo.[J]. Arch Toxicol. 2020;94:3329–42. Kay N, Huang C-Y, Shiu L-Y, Yu Y-C, et al. The effects of anti-TGF-β1 on epithelial-mesenchymal transition in the pathogenesis of adenomyosis.[J]. Reprod Sci. 2020;27:1698–706. Maschio Daniela A, Matheus Valquíria A, Collares-Buzato CB. Islet cells are the source of Wnts that can induce beta-cell proliferation in vitro.[J]. J Cell Physiol. 2019;234:19852–65. Tenjin Y, Kudoh S, Kubota S, Yamada T, Matsuo A, et al. Ascl1-induced Wnt11 regulates neuroendocrine differentiation, cell proliferation, and E-cadherin expression in small-cell lung cancer and Wnt11 regulates small-cell lung cancer biology.[J]. Lab Investig. 2019;99:1622–35. Li J, Yanyan M, Mu L, et al. The expression of Bcl-2 in adenomyosis and its effect on proliferation, migration, and apoptosis of endometrial stromal cells. Pathol Res Pract. 2019;215(08):152477. Di Leva G, Garofalo M, Croce CM. MicroRNAs in cancer. Annual Rev Pathology. 2014;9(1):287–314. Mutlu M, Raza U, Saatci O, Eyupoglu E, et al. miR-200c: a versatile watchdog in cancer progression, EMT, and drug resistance.[J]. J Mol Med. 2016;94:629–44. Zhang W, Mao Y-Q, Wang H, et al. MiR-124 suppresses cell motility and adhesion by targeting talin 1 in prostate cancer cells.[J]. Cancer Cell Int. 2015;15:49. Gao J, Yin X-B, Yu X, et al. Long noncoding RNA LINC00488 functions as a ceRNA to regulate hepatocellular carcinoma cell growth and angiogenesis through miR-330-5.[J]. Dig Liver Dis. 2019;51(7):1050–9. Tang H-Y, Liu Y, Cheng W, et al. microRNA-96-5p induces the epithelial-mesenchymal transition to promote the metastasis of hepatocellular carcinoma by post-transcriptionally downregulating Talin 1.[J]. Int J Clin Exp Pathol. 2019;12(5):1897–908. Li X-Z, Sun Y-L, Huang S-L, et al. Inhibition of AZIN2-sv induces neovascularization and improves prognosis after myocardial infarction by blocking ubiquitin-dependent talin1 degradation and activating the Akt pathway.[J]. EBioMedicine. 2019;39:69–82. Hua M-H, Qin Y-W, Sheng M-H, Cui X-P, et al. miR-145 suppresses ovarian cancer progression via modulation of cell growth and invasion by targeting CCND2 and E2F3.[J]. Mol Med Rep. 2019;19:3575–83. Zhang X-F, Zhang X-Q, Chang Z-X, et al. microRNA-145 modulates migration and invasion of bladder cancer cells by targeting N-cadherin.[J]. Mol Med Rep. 2018;17:8450–6. Funding This study was funded by the National Key Research and Development Program of China (2018YFC1004803) and was supported by grants from the National Natural Science Foundation of China (No. 81571412). Author information Authors and Affiliations Corresponding author Ethics declarations Conflict of Interest The authors declare that they have no conflict of interest. Additional information Publisher’s Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Supplementary Information ESM 1 (download DOCX ) (DOCX 319 kb) Rights and permissions About this article Cite this article Wang, Yy., Duan, H., Wang, S. et al. Talin1 Induces Epithelial-Mesenchymal Transition to Facilitate Endometrial Cell Migration and Invasion in Adenomyosis Under the Regulation of microRNA-145-5p. Reprod. Sci. 28, 1523–1539 (2021). https://doi.org/10.1007/s43032-020-00444-8 Received: Accepted: Published: Version of record: Issue date: DOI: https://doi.org/10.1007/s43032-020-00444-8

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adenomyosis

MeSH descriptors

Adenomyosis Cell Movement Cell Movement Endometrium Epithelial-Mesenchymal Transition Epithelial-Mesenchymal Transition MicroRNAs Talin Adenomyosis Adenomyosis Endometrium Endometrium Endometrium Female Female Humans Humans MicroRNAs MicroRNAs Primary Cell Culture

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