Effects of metformin on cell viability and inflammatory status of human colonocytes: an in vitro preliminary analysis.
- 1Department of Surgery, Medicine, Dentistry and Morphological Sciences with Interest in Transplant, Oncology and Regenerative Medicine, University of Modena and Reggio Emilia, Modena, Italy.
- 2Department of Medical and Surgical Sciences, University of Modena and Reggio Emilia, Modena, Italy.
Abstract
Metformin exerts anticancer effects by targeting various cancer cells while also providing anti-inflammatory and antioxidant benefits. Inflammation is a complex process involving the release of soluble factors such as cytokines. Among these, IL-6 plays a pivotal role in mediating chronic inflammation and promoting tumour growth, thereby contributing to cancer progression. Patients with advanced or metastatic colon cancer exhibit elevated serum IL-6 levels. The autophagic process serves a dual role in colorectal carcinogenesis, partly promoting and partly inhibiting tumour growth. However, there are currently no reliable data on the role of autophagy in colorectal cancer. The present study evaluated the impact of metformin on normal human colonic cells. The viability of colonocytes from healthy donors was assessed, and the effects of metformin on inflammation and autophagy were investigated using immunofluorescence, western blot analysis, and real-time PCR evaluation of MAPLC3, IL-6, and BCL2 mRNA expression levels. Metformin did not affect the viability of normal colonocytes. Moreover, it exerted both anti-inflammatory and anti-autophagic effects on these cells, as evidenced by downregulation of IL-6 and MAPLC3 expression at both the protein and mRNA levels, while maintaining cell viability as shown by BCL2 expression. These observations support the hypothesis of cellular selectivity of metformin, suggesting that it may exert differential effects on cancer versus normal cells. Metformin appears to attenuate autophagy in healthy cells while potentially driving apoptosis or autophagy in tumour cells, representing a strategy to minimise damage to normal tissue while effectively targeting cancerous cells.
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BibTeX
@article{orlandi2026effects,
title = {{Effects of metformin on cell viability and inflammatory status of human colonocytes: an in vitro preliminary analysis.}},
author = {Giulia Orlandi and Luca Roncucci and Monica Pedroni and Paola Sena},
journal = {Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology},
year = {2026},
month = nov,
doi = {10.5603/rpor.113084},
url = {https://europepmc.org/article/MED/42997866},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Effects of metformin on cell viability and inflammatory status of human colonocytes: an in vitro preliminary analysis.
AU - Giulia Orlandi
AU - Luca Roncucci
AU - Monica Pedroni
AU - Paola Sena
PY - 2026
DA - 2026/11/01
JO - Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology
DO - 10.5603/rpor.113084
UR - https://europepmc.org/article/MED/42997866
AB - Metformin exerts anticancer effects by targeting various cancer cells while also providing anti-inflammatory and antioxidant benefits. Inflammation is a complex process involving the release of soluble factors such as cytokines. Among these, IL-6 plays a pivotal role in mediating chronic inflammation and promoting tumour growth, thereby contributing to cancer progression. Patients with advanced or metastatic colon cancer exhibit elevated serum IL-6 levels. The autophagic process serves a dual role in colorectal carcinogenesis, partly promoting and partly inhibiting tumour growth. However, there are currently no reliable data on the role of autophagy in colorectal cancer. The present study evaluated the impact of metformin on normal human colonic cells. The viability of colonocytes from healthy donors was assessed, and the effects of metformin on inflammation and autophagy were investigated using immunofluorescence, western blot analysis, and real-time PCR evaluation of MAPLC3, IL-6, and BCL2 mRNA expression levels. Metformin did not affect the viability of normal colonocytes. Moreover, it exerted both anti-inflammatory and anti-autophagic effects on these cells, as evidenced by downregulation of IL-6 and MAPLC3 expression at both the protein and mRNA levels, while maintaining cell viability as shown by BCL2 expression. These observations support the hypothesis of cellular selectivity of metformin, suggesting that it may exert differential effects on cancer versus normal cells. Metformin appears to attenuate autophagy in healthy cells while potentially driving apoptosis or autophagy in tumour cells, representing a strategy to minimise damage to normal tissue while effectively targeting cancerous cells.
SN - 1507-1367
SN - 2083-4640
ER -