V.parvula regulates JAK2-STAT3 to promote colorectal cancer

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Veillonella parvula enhances complement C3 expression in colonic tissue, activating the JAK2-STAT3 signaling pathway and promoting colorectal cancer development in a mouse model and human cell lines.

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The study investigated how Veillonella parvula contributes to colorectal cancer, using a colorectal cancer mouse model supplemented with V. parvula to assess effects on intestinal tumor number and size, alongside RNA-seq and Western blot analyses of relevant molecules. The researchers found that V. parvula–treated mice had increased intestinal tumors and showed elevated expression of complement C3 and the C3a receptor in colonic tissues. In two human colorectal cancer cell lines, exogenous C3 activated the JAK2–STAT3 signaling pathway, and this activation was attenuated by the JAK2 inhibitor AG490. A major limitation is that the work is presented as a preprint and has not been peer reviewed. The paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

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Abstract

Background: The dysregulation of the gut microbiota is associated with the occurrence and development of colorectal cancer. Several clinical studies have indicated that the abundance of Veillonella parvula in the intestines of colorectal cancer patients is higher than that in the normal population. The aim of this study is to explore the mechanisms through which Veillonella parvula promotes colorectal cancer. Methods: Establish a colorectal cancer mouse model to assess the tumor-promoting effect of Veillonella parvula. Utilize RNA-seq, Western blot, and other techniques to examine the expression of relevant molecules. Furthermore, employ two human colorectal cancer cell lines in vitro to validate the relationship between complement C3 and the JAK2-STAT3 signaling pathway. Results: In comparison to the control group, mice administered with Veillonella parvula exhibited an increased number and size of intestinal tumors. Furthermore, a significant enhancement in the expression of C3 and C3a receptor proteins was noted in the colorectal tissues of mice treated with Veillonella parvula. The results from in vitro experiments indicated that the addition of exogenous C3 in the culture of colorectal cancer cells activated the JAK2 - STAT3 signaling pathway. The activation was attenuated upon the introduction of the JAK2 inhibitor AG490. Conclusion: Veillonella parvula enhances complement C3 expression in colonic tissue, activating the JAK2-STAT3 signaling pathway and promoting colorectal cancer development.
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V.parvula regulates JAK2-STAT3 to promote colorectal cancer | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article V.parvula regulates JAK2-STAT3 to promote colorectal cancer Xuhao Bai, jiaxin Deng, jiawei zhang, qinghua zhong, dezheng lin, and 7 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-4079469/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 4 You are reading this latest preprint version Abstract Background: The dysregulation of the gut microbiota is associated with the occurrence and development of colorectal cancer. Several clinical studies have indicated that the abundance of Veillonella parvula in the intestines of colorectal cancer patients is higher than that in the normal population. The aim of this study is to explore the mechanisms through which Veillonella parvula promotes colorectal cancer. Methods: Establish a colorectal cancer mouse model to assess the tumor-promoting effect of Veillonella parvula. Utilize RNA-seq, Western blot, and other techniques to examine the expression of relevant molecules. Furthermore, employ two human colorectal cancer cell lines in vitro to validate the relationship between complement C3 and the JAK2-STAT3 signaling pathway. Results: In comparison to the control group, mice administered with Veillonella parvula exhibited an increased number and size of intestinal tumors. Furthermore, a significant enhancement in the expression of C3 and C3a receptor proteins was noted in the colorectal tissues of mice treated with Veillonella parvula. The results from in vitro experiments indicated that the addition of exogenous C3 in the culture of colorectal cancer cells activated the JAK2 - STAT3 signaling pathway. The activation was attenuated upon the introduction of the JAK2 inhibitor AG490. Conclusion: Veillonella parvula enhances complement C3 expression in colonic tissue, activating the JAK2-STAT3 signaling pathway and promoting colorectal cancer development. Colorectal cancer Veillonella parvula Complement C3 JAK2 STAT3 Full Text Cite Share Download PDF Status: Under Review Version 1 posted Reviewers agreed at journal 25 Mar, 2024 Reviewers invited by journal 25 Mar, 2024 Editor assigned by journal 13 Mar, 2024 First submitted to journal 11 Mar, 2024 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. 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