Butyrate, a postbiotic of intestinal bacteria, affects pancreatic cancer and gemcitabine response in in vitro and in vivo models

Panebianco, Concetta; Villani, Antonio; Pisati, Federica; Orsenigo, Fabrizio; Ulaszewska, Marynka; Latiano, Tiziana Pia; Potenza, Adele; Andolfo, Annapaola; Terracciano, Fulvia; Tripodo, Claudio; Perri, Francesco; Pazienza, Valerio

doi:10.1016/j.biopha.2022.113163

Cited by 59 publications

(49 citation statements)

References 57 publications

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“…Furthermore, treating pancreatic carcinoma cell lines with sodium butyrate increases cell sensitivity to SN-38, cisplatin, and fluorouracil chemotherapies by inducing histone acetylation and p53 expression and subsequently increasing apoptosis [ 58 ]. A similar synergic effect was also observed after combined butyrate treatment with docetaxel, irinotecan, gemcitabine, or cisplatin both in vitro and in vivo against various types of tumors [ 45 , 46 , 47 , 59 ]. The co-administration of docetaxel and butyrate enhanced docetaxel response by upregulation and downregulation of apoptosis and proliferation-related proteins, respectively, [ 59 ].…”

Section: Scfas and Cancer Treatment Responsementioning

confidence: 55%

“…Further, butyrate reduced irinotecan’s half maximal inhibitory concentration, expression of the chemoresistant-related protein P-glycoprotein and enhanced cancer cell apoptosis and anti-tumor efficiency of irinotecan against colon cancer cell lines [ 45 ]. Combined gemcitabine and butyrate treatment also further prompted apoptosis and reduced tumor-associated stromatogenesis in pancreatic ductal adenocarcinoma models [ 46 ]. Additionally, butyrate enhanced tumor apoptosis and the suppression of tumor growth, migration, and invasion capacity of gastric cancer cell lines treated with cisplatin [ 47 ] ( Figure 2 ).…”

Section: Scfas and Cancer Treatment Responsementioning

confidence: 99%

“…SCFAs may also help protect against GI toxicity of gemcitabine, a standard treatment for pancreatic cancer. It has been shown that, in a pancreatic cancer mouse model treated with gemcitabine, butyrate supplements can reduce intestinal injury by preserving villi structure, increasing mucin production, enriching butyrate and propionate-producing bacteria, and suppressing pro-inflammatory microbes [ 46 ].…”

Section: Scfas and Cancer Treatment Toxicitiesmentioning

confidence: 99%

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Gut Microbiota-Derived Short-Chain Fatty Acids: Impact on Cancer Treatment Response and Toxicities

et al. 2022

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The gut microbiota has emerged as a key modulator of cancer treatment responses in terms of both efficacy and toxicity. This effect is clearly mediated by processes impacting the activation and modulation of immune responses. More recently, the ability to regulate chemotherapeutic drug metabolism has also emerged as a key driver of response, although the direct mechanisms have yet to be fully elucidated. Through fermentation, the gut microbiota can produce several types of metabolites, including short-chain fatty acids (SCFAs). SCFAs play an important role in maintaining epithelial barrier functions and intestinal homeostasis, with recent work suggesting that SCFAs can modulate response to cancer treatments and influence both anti-tumor immune response and inflammatory-related side effects. In this review, we will discuss the importance of SCFAs and their implications for cancer treatment response and toxicities.

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Section: Scfas and Cancer Treatment Responsementioning

confidence: 55%

Section: Scfas and Cancer Treatment Responsementioning

confidence: 99%

Section: Scfas and Cancer Treatment Toxicitiesmentioning

confidence: 99%

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Gut Microbiota-Derived Short-Chain Fatty Acids: Impact on Cancer Treatment Response and Toxicities

et al. 2022

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“…FMT and postbiotics are promising potential therapies, especially for relapsing diseases, because of their relatively fewer side effects and low toxicity levels ( Yoshimatsu et al., 2015 ; Salminen et al., 2021 ; Mendelsohn et al., 2022 ). Butyrate has been considered as a postbiotic ( Panebianco et al., 2022 ). The colon is the main site at which butyric acid absorption and gut microbiological colonization occur.…”

Section: Discussionmentioning

confidence: 99%

Sodium butyrate treatment and fecal microbiota transplantation provide relief from ulcerative colitis-induced prostate enlargement

Dong

Zheng²,

Huang³

et al. 2022

Front. Cell. Infect. Microbiol.

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The ability to regulate the gut environment has resulted in remarkable great breakthroughs in the treatment of several diseases. Several studies have found that the regulation of the gut environment might provide relief from the symptoms of benign prostatic hyperplasia. However, the correlation between the gut microenvironment and the colon and prostate glands is still unknown. We found that ulcerative colitis (UC) induced an increase in prostate volumes that could be reversed by sodium butyrate (NaB) and fecal microbiota transplantation (FMT). The mechanism by which UC induced changes in the prostate gland was examined via RNA-Seq. The results show that the expression level of GPER was significantly lower in the prostate gland of UC mices than in normal mices. The expression of GPER could be increased via treatment with NaB or FMT. We found that prostate tissues exhibited higher butryic acid levels after they were treated with NaB or FMT. In experiments conducted in vitro, NaB or the fecal filtrate (FF) from healthy mice up-regulated of the expression of GPER, inhibited cell growth, and induced apoptosis in BPH-1 cells. These changes could be alleviated by treatment with the G15 or in GPER-silenced cells.

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“…Panebianco et al described that butyrate treatment affected lipidome and metabolome in pancreatic cancer nude BALB/c mice. In addition, butyrate supplementation led to an increase in saturated palmitic acid and stearic acid in gemcitabine-treated mice (63). High expression of aryl hydrocarbon receptor (AhR) correlated with cancer progression.…”

Section: Pancreatic Tumor Microbiomementioning

confidence: 99%

Tumor microbiome – an integral part of the tumor microenvironment

et al. 2022

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The tumor microenvironment (TME) plays a significant role in tumor progression and cancer cell survival. Besides malignant cells and non-malignant components, including immune cells, elements of the extracellular matrix, stromal cells, and endothelial cells, the tumor microbiome is considered to be an integral part of the TME. Mounting evidence from preclinical and clinical studies evaluated the presence of tumor type-specific intratumoral bacteria. Differences in microbiome composition between cancerous tissues and benign controls suggest the importance of the microbiome-based approach. Complex host-microbiota crosstalk within the TME affects tumor cell biology via the regulation of oncogenic pathways, immune response modulation, and interaction with microbiota-derived metabolites. Significantly, the involvement of tumor-associated microbiota in cancer drug metabolism highlights the therapeutic implications. This review aims to summarize current knowledge about the emerging role of tumor microbiome in various types of solid malignancies. The clinical utility of tumor microbiome in cancer progression and treatment is also discussed. Moreover, we provide an overview of clinical trials evaluating the role of tumor microbiome in cancer patients. The research focusing on the communication between the gut and tumor microbiomes may bring new opportunities for targeting the microbiome to increase the efficacy of cancer treatment and improve patient outcomes.

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Butyrate, a postbiotic of intestinal bacteria, affects pancreatic cancer and gemcitabine response in in vitro and in vivo models

Cited by 59 publications

References 57 publications

Gut Microbiota-Derived Short-Chain Fatty Acids: Impact on Cancer Treatment Response and Toxicities

Gut Microbiota-Derived Short-Chain Fatty Acids: Impact on Cancer Treatment Response and Toxicities

Sodium butyrate treatment and fecal microbiota transplantation provide relief from ulcerative colitis-induced prostate enlargement

Tumor microbiome – an integral part of the tumor microenvironment

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