Clostridium butyricum (C.B), as a probiotic, has been found to play a supporting role in colorectal cancer treatment (CRC), according to a recent study by Professor Li Menghong's team at the Institute of Gastroenterology, The Sixth Affiliated Hospital, Sun Yat-sen University.

(Photo provided to GDToday)

The study was published on Gut Microbes under the title "Therapeutic potential of Clostridium butyricum anticancer effects in colorectal cancer".

Colorectal cancer is one of the deadliest cancer types with strong resistance to various therapies, and is a cancer type with a very high mortality rate. 

The important advances in microbiome studies have characterized the critical protecting role of intestinal microbes, such as probiotics, in human cancers. Probiotic bacteria impact physiological and immunological mechanisms; therefore, they may have antitumor activities.

However, the impacts of many probiotics on cancer development remain to be characterized. 

Schematic summary of C.B's role in modulating 5-FU (one of the most commonly used drugs to treat cancer) drug resistance and boosting anti-PD1 immunotherapy. (Photo provided to GDToday)

The team discovered that C.B regulates cell proliferation, patient-derived organoid (PDO) growth, and metastases in CRC. C.B is involved in regulating MYC (a family of regulator genes and proto-oncogenes that consist of three human genes: c-MYC, l-MYC, and n-MYC) ubiquitination and destabilization.

C.B antagonizes MYC-mediated expression of TYMS (Thymidine Synthesase), thus sensitizing 5-FU treatment efficacy. C.B potentiates 5-FU treatment in a xenograft mouse model. Therapeutic benefits of C.B involve MYC downregulation and increased CD8+ T cell infiltration, thereby boosting anti-PD1 therapeutic efficacy.

The findings uncover previously unappreciated links between C.B and CRC cell signaling, providing insight into the tumorigenesis modulating mechanisms of C.B in boosting chemo/immune therapies.

Group photo of Professor Li Menghong's research team. (Photo provided to GDToday)