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Molecular and Immunological Research on Colorectal Cancer: Pathogenesis, Microenvironment, and Future Therapies

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Dr. Mónica G Mendoza-Rodríguez

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Unidad de Investigación en Biomedicina, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Avenida de los Barrios 1, Los Reyes Iztacala, Tlalnepantla 54090, Mexico
Interests: colorectal cancer pathogenesis; helminth infections and cancer; immunology and inflammation; biotherapeutic development

Special Issue Information

Dear Colleagues,

Colorectal cancer (CRC) is a significant global health concern, driven by intricate interactions among genetic, epigenetic, immunological, and environmental factors. This Special Issue seeks to showcase recent advances in understanding the molecular mechanisms of CRC pathogenesis and progression, including the aggressive behavior of cancer cells. We also aim to highlight research on tumor microenvironment dynamics, inflammation-related signaling pathways, and the influence of microorganisms on chemotherapy response. We welcome original research and review articles that investigate novel biomarkers, therapeutic targets, and biotherapeutic strategies, as well as studies exploring immune modulation and the role of microbiota in CRC development. By embracing multidisciplinary perspectives, this issue aspires to deepen our understanding of CRC biology and inspire innovative approaches to its diagnosis, treatment, and prevention.

Dr. Mónica G Mendoza-Rodríguez
Guest Editor

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27 pages, 4553 KB

Open AccessArticle

Dihydroartemisinin Unravels Dose-Dependent Transcriptomic Networks Orchestrating Ferroptosis and Metabolic Reprogramming in Colorectal Cancer

by Zhaodi Zheng, Xitan Hou, Wenjuan Li and Leilei Zhang

Curr. Issues Mol. Biol. 2026, 48(4), 342; https://doi.org/10.3390/cimb48040342 - 25 Mar 2026

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Abstract

Background/Objectives: Dihydroartemisinin (DHA), a bioactive metabolite of Artemisia annua, displays potent antitumor activity in multiple cancers. However, its dose-dependent transcriptional regulatory networks in colorectal cancer (CRC) remain insufficiently understood. This study aimed to clarify the molecular mechanisms of low- and high-dose DHA in human CRC cells and reveal the dose-dependent crosstalk among related biological processes. Methods: We integrated RNA-seq transcriptomic profiling and functional validation in HCT116 cells treated with 20 μM (low-dose) or 50 μM (high-dose) DHA. Differentially expressed genes (DEGs) were screened at FDR ≤ 0.05 and |log₂(fold change)| ≥ 1, followed by GO and KEGG enrichment analyses. Results: DHA inhibited cell viability dose-dependently, with an IC₅₀ of 50 μM. We identified 280 and 678 DEGs in low-and high-dose groups, respectively. Low-dose DHA induced apoptosis via GADD45α/β and ATF4/DDIT3-mediated endoplasmic reticulum stress and triggered senescence through G2/M phase arrest. High-dose DHA mainly modulated gene expression signatures associated with ferroptosis by regulating iron homeostasis and lipid peroxidation at the transcriptional level. Both doses suppressed glycolysis, lipid, and folate metabolism; high-dose DHA also inhibited MGAT5B-mediated glycosylation. DHA regulated five core signaling pathways dose-dependently, with high-dose DHA further repressing Wnt3a/16 and BMP4/6. Conclusions: This study first identifies ferroptosis-related gene networks as key transcriptional targets. It reveals dose-dependent crosstalk among cell death, senescence, metabolic reprogramming, and signaling, providing a transcriptomic framework and gene targets for optimizing DHA-based colorectal cancer therapy. Full article

(This article belongs to the Special Issue Molecular and Immunological Research on Colorectal Cancer: Pathogenesis, Microenvironment, and Future Therapies)

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16 pages, 8077 KB

Open AccessArticle

The Senescence-SASP Landscape in Colon Adenocarcinoma: Prognostic and Therapeutic Implications

by Tianyu Ren, Suyouwei Gao, Yangrong Feng, Yangyang Xu, Xinyi Mi, Jite Shi and Man Chu

Curr. Issues Mol. Biol. 2026, 48(1), 114; https://doi.org/10.3390/cimb48010114 - 21 Jan 2026

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Abstract

Cellular senescence, characterized by permanent cell cycle arrest, significantly influences cancer development, immune regulation, and progression. However, the precise mechanisms by which senescence contributes to colorectal cancer prognosis remain to be fully elucidated. By integrating expression profiles of senescence-related and prognostic genes in colon adenocarcinoma (COAD) patients, we formulated and confirmed a nine-gene cellular senescence-related signature (CSRS) that integrates senescence-associated and prognosis-predictive genes using data from the CellAge, The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO). A cell senescence-related prognostic formula was developed as follows: CSRS = (CASP2 × 0.2098) + (CDKN2A × 0.1196) + (FOXD1 × 0.1472) + (ING5 × 0.3723) + (OXTR × 0.0786) + (PHGDH × 0.1408) + (SERPINE1 × 0.1127) + (SNAI1 × 0.1034) + (LIMK1 × 0.0747). In a multivariate Cox proportional hazards model, the CSRS score, age and TNM stage were all identified as significant independent indicators for overall survival, affirming their prognostic value in colorectal cancer. The CSRS-high group exhibited significantly up-regulated senescence-associated secretory phenotype (SASP) and immune cell infiltration, whereas the CSRS-low group showed an apparent better response to immune-checkpoint inhibitor therapy. Our findings suggest CSRS score and its constituent genes represent potential biomarkers for prognosis and immunotherapeutic benefit in COAD patients. Extending this nine-gene set into a broader senescence-associated panel should be a next step toward delivering truly individualized treatment plans. Full article

(This article belongs to the Special Issue Molecular and Immunological Research on Colorectal Cancer: Pathogenesis, Microenvironment, and Future Therapies)

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