Life Sciences Student Journal https://journals.fmsbi.com/LSSJ <p>The <em>Life Sciences Student Journal (LSSJ)</em> <a href="https://portal.issn.org/resource/ISSN/2980-9592">ISSN 2980-9592</a> is an open-access journal publishing across the entire range of Bio-science research on the basis of objective peer-review. The journal allows early-career scientists to publish high-quality articles it receives without the usual restrictions on the scope. The <em>Life Sciences Student Journal </em>covers the entire range of biological science and therefore, LSSJ welcomes the submission of all high-quality bio-science research including articles that may usually be difficult to publish elsewhere. LSSJ publishes in the Continuous Article Publication (CAP) model.</p> <p>Index: </p> <p><a href="https://www.sudoc.fr/271648724"><img src="https://journals.fmsbi.com/public/site/images/nourani/mceclip0-6c0c520b45ca651085dae598b2bd7707.png" /> <img src="https://journals.fmsbi.com/public/site/images/nourani/mceclip0-c0f363bfb79fa35348937780f466ae46.png" /> </a></p> <p><img src="https://journals.fmsbi.com/public/site/images/nourani/ic-1.jpg" alt="" width="200" height="51" /> <a href="https://journalseeker.researchbib.com/view/issn/2980-9592"><img src="https://www.researchbib.com/sites/image/logo.png" alt="ResearchBib" width="102" height="46" /></a></p> <p><a href="https://civilica.com/l/182109/"><img src="https://journals.fmsbi.com/public/site/images/nourani/civilica.jpg" alt="" width="149" height="52" /></a><a href="https://www.sid.ir/journal/43116/en"><img src="https://journals.fmsbi.com/public/site/images/nourani/sid-logo70p.png" alt="" width="70" height="38" /></a></p> Frontier Medical Systems Biology Inc en-US Life Sciences Student Journal 2980-9592 <h3> Publisher's Own License</h3> <p>This work is licensed under the publisher's own license, which allows for sharing and use under specific conditions. <strong>Attribution</strong> is required; users must give appropriate credit to the original creator. Additionally, this license includes a <strong>No Commercial Usage</strong> clause, meaning that the work cannot be used for commercial purposes or for profit. Users are encouraged to share and adapt the content non-commercially, provided they adhere to these guidelines. Please ensure that you respect the terms of this license to promote a collaborative and respectful use of the work.</p> Postbiotics as Modulators of Apoptotic and Metastatic Pathways in Colorectal Cancer: Insights from HT-29 Cell Responses https://journals.fmsbi.com/LSSJ/article/view/170 <p>Colorectal cancer is one of the leading causes of cancer-related morbidity and mortality worldwide, and its incidence is strongly influenced by diet, lifestyle, chronic inflammation, and the composition of the gut microbiota.[1–4] Increasing evidence suggests that microbial dysbiosis contributes to tumor initiation and progression through altered metabolite production, impaired barrier function, and activation of oncogenic signaling pathways such as Wnt/β-catenin, NF-κB, MAPK/ERK, and STAT3.[3,5,6,14,19] In parallel, interest has grown in microbiota-centered interventions, particularly probiotics, prebiotics, synbiotics, and more recently postbiotics, which are defined as non-viable microbial cells, components, or metabolites that exert health-promoting effects in the host.[3,7–10] Postbiotics are attractive because they are stable, safe for immunocompromised patients, and easier to standardize than live probiotics, while still retaining potent immunomodulatory, anti-inflammatory, and anticancer activities.[7–13,21,26] Experimental and review data indicate that postbiotics can inhibit CRC cell growth, induce apoptosis, modulate the cell cycle, and regulate metastasis-associated genes and pathways, including <em>RSPO2, NGF, MMP7</em>, and mitochondrial apoptosis regulators such as <em>Bax, Bcl-2</em>, and caspase-3.[10–13,16,17,20] In particular, postbiotics derived from <em>Bifidobacterium breve</em> and <em>Lactobacillus rhamnosus</em> have shown promising effects in HT-29 colorectal cancer cells, where they promote apoptosis and attenuate pro-metastatic gene expression.[10,20] This review summarizes current knowledge on the relationship between the gut microbiota and CRC, defines and contextualizes postbiotics, explores their molecular mechanisms in carcinogenesis with a focus on CRC, and discusses the translational and clinical potential of postbiotics as complementary tools in CRC prevention and management.[3,7,11–13,18,26–28]</p> Hiva safaei Copyright (c) 2025 Life Sciences Student Journal 2025-12-06 2025-12-06 3 4 1 13 10.22034/LSSJ.2025.170