The imbalance in the gut microbiome plays a vital role in the progression of many diseases, including cancer, due to increased inflammation in the body. Since gut microbiome-induced inflammation can serve as a novel therapeutic strategy, there is an increasing need to identify novel approaches to investigate the effect of inflammation instigated by gut microbiome on cancer cells. However, there are limited biomimetic co-culture systems that allow testing of the causal relationship of the microbiome on cancer cells. Here we developed a microfluidic chip that can simulate the interaction of the gut microbiome and cancer cells to investigate the effects of bacteria and inflammatory stress on cancer cells in vitro. To test the microfluidic chip, we used colorectal cancer cells, as an increased microbiome abundance has been associated with poor outcomes in colorectal cancer. We cultured colorectal cancer cells with Bacillus bacteria or lipopolysaccharide (LPS), a purified bacterial membrane that induces a significant inflammatory response, in the microfluidic device. Our results showed that both LPS and Bacillus significantly accelerated the growth of colorectal cancer cells, therefore supporting that the increased presence of certain bacteria promotes cancer cell growth. The microfluidic device included in this study may have significant implications in identifying new treatments for various cancer types in the future.
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http://dx.doi.org/10.3390/s23031265 | DOI Listing |
Discov Oncol
January 2025
Department of General Surgery, The Second Affiliated Hospital of the Air Force Medical University, Xi'an, 710038, China.
A common digestive system cancer with a dismal prognosis and a high death rate globally is breast cancer (BRCA). BRCA recurrence, metastasis, and medication resistance are all significantly impacted by cancer stem cells (CSCs). However, the relationship between CSCs and the tumor microenvironment in BRCA individuals remains unknown, and this information is critically needed.
View Article and Find Full Text PDFAdv Sci (Weinh)
January 2025
Department of Pharmacology, School of Pharmacy, China Medical University, Shenyang, 110122, China.
Hydrogen sulfide (HS)-mediated protein S-sulfhydration has been shown to play critical roles in several diseases. Tumor-associated macrophages (TAMs) are the predominant population of immune cells present within solid tumor tissues, and they function to restrict antitumor immunity. However, no previous study has investigated the role of protein S-sulfhydration in TAM reprogramming in breast cancer (BC).
View Article and Find Full Text PDFNaunyn Schmiedebergs Arch Pharmacol
January 2025
Department of Respiratory and Critical Care Medicine, Guangdong Provincial Hospital of Traditional Chinese Medicine, No. 111, Dade Road, Guangzhou, 510120, China.
Berberine (BBR) has been proved to inhibit the malignant progression of non-small cell lung cancer (NSCLC), but the underlying molecular mechanism still needs to be further revealed. NSCLC cells (A549 and H1299) were treated with BBR. CCK8 assay, colony formation assay, flow cytometry, TUNEL staining and transwell assay were used to examine cell proliferation, apoptosis and invasion.
View Article and Find Full Text PDFApoptosis
January 2025
Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai, China.
Cancer-associated fibroblasts (CAFs) significantly influence tumor progression and therapeutic resistance in colorectal cancer (CRC). However, the distributions and functions of CAF subpopulations vary across the four consensus molecular subtypes (CMSs) of CRC. This study performed single-cell RNA and bulk RNA sequencing and revealed that myofibroblast-like CAFs (myCAFs), tumor-like CAFs (tCAFs), inflammatory CAFs (iCAFs), CXCL14CAFs, and MTCAFs are notably enriched in CMS4 compared with other CMSs of CRC.
View Article and Find Full Text PDFBull Math Biol
January 2025
CFisUC, Department of Physics, University of Coimbra, Rua Larga, 3004-516, Coimbra, Portugal.
Hereditary diffuse gastric cancer is characterized by an increased risk of diffuse gastric cancer and lobular breast cancer, and is caused by pathogenic germline variants of E-cadherin and -E-catenin, which are key regulators of cell-cell adhesion. However, how the loss of cell-cell adhesion promotes cell dissemination remains to be fully understood. Therefore, a three-dimensional computer model was developed to describe the initial steps of diffuse gastric cancer development.
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