ArticleIEEE open journal of engineering in medicine and biology2026
MicroRNA-873 Suppresses Viability and Invasion of Colorectal Cancer Through KRAS/MAPK Signaling and Sensitizes Tumor Spheroids to 5-Fluorouracil in a 3D Microwell Model.
Article in IEEE open journal of engineering in medicine and biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- microRNAs as Regulators of the Immune Response and Their Potential Therapeutic Applications in Cancer.Non-coding RNA · 2026Review
- Evaluating KRAS-Associated Responses to Sulfasalazine and 5-Fluorouracil in Colorectal Cancer Using Integrated 2D and PEGDA Microwell-Based 3D Tumor Models.International journal of molecular sciences · 2026Article
- Hybrid Neural Network Architecture for Automated Liver and Tumor Segmentation Using Ensemble Learning on CT Images.Biomimetics (Basel, Switzerland) · 2026Article
- Tumor-Suppressive microRNA Therapy Inhibits Growth of Glioblastoma Multiforme Xenografts.Cancers · 2026Article
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5 authors.
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Abstract
Colorectal cancer (CRC) ranks third in incidence among all malignancies and is highly lethal in advanced stages. Combination chemotherapy regimens based on 5-fluorouracil (5-FU) remain the mainstay of colorectal cancer treatment alongside surgical resection. Even though new treatment modalities are emerging, many are either ineffective against KRAS-mutant tumors or prone to therapy resistance. Therefore, there is a critical need for new targeted therapies that may overcome the KRAS-driven chemoresistance and enhance the effect of chemotherapy. MicroRNAs can modulate several oncogenic pathways at once and can strengthen chemotherapy. In this study, we identified miR-873 as a potential chemosensitizer that modulates KRAS/MAPK signaling in CRC. We found that KRAS is overexpressed in metastatic versus primary tissues and in a large CRC patient cohort (n 1,061), high KRAS expression was associated with worse overall survival (HR 1.27; 95 CI, 1.041.56; log-rank p 0.018). In vitro inhibition of KRAS by siRNA reduced clonogenic growth (HCT116, p 0.0023; RKO, p 0.0018) and invasion (p 0.0001). In silico prediction (TargetScan/miRWalk) analyses showed a conserved binding site between miR-873 and KRAS 3UTR. Consistent with this prediction, miR-873 mimic transfection reduced KRAS protein expression and phenocopied KRAS knockdown by suppressing colony formation (p 0.0021) and invasion (p 0.0001) in KRAS-mutant HCT116 and KRAS-wild-type RKO cells. Dose-matrix screening and SynergyFinder+ analysis revealed synergistic inhibition of spheroid viability with miR-873 + 5-FU, including a low-dose pair (25 nM miR-873 + 12.5 M 5-FU) showing positive synergy across ZIP/HSA/Bliss/Loewe models. In a poly(ethylene glycol)diacrylate(PEGDA) microwell 3D platform that generates uniform, size-controlled CRC spheroids, this combination produced the strongest suppression of spheroid expansion (day-5/day-3 area: HCT116, 0.61 0.18 vs control, 2.08 0.49; RKO, 0.66 0.04 vs control, 2.08 0.31) and reduced the live-cell fraction to 41 in both lines. Moreover, western blot analysis showed decreased KRAS and MAPK pathway activity (reduced p-ERK and context-dependent p-MEK), reduced Cyclin D1, and increased apoptotic readouts (cleaved PARP and a Bax/Bcl-2 shift). Together, these results position miR-873 treatment as a potential targeting approach to suppress KRAS/MAPK signaling and sensitize CRC to 5-FU and validate our PEGDA microwell 3D platform as a practical, translational testbed for miRNAchemotherapy combinations.
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