Gut butyrate-producing organisms correlate to Placenta Specific 8 protein: importance to colorectal cancer progression

Chi-Cheng Huang, Ming-Hung Shen, Shao-Kuan Chen, Shung-Haur Yang, Chih-Yi Liu, Jiun-Wen Guo, Kang-Wei Chang, Chi-Jung Huang

Research output: Contribution to journalArticle

Abstract

Tumor metastasis or recurrence often occurs in patients with curative resection of colorectal cancer (CRC). Placental-specific 8 (PLAC8), which has increased expression in stool, may be associated with CRC recurrence. Insights into the role of PLAC8 in CRC recurrence and its clinical significance may support to develop strategies for preventing CRC recurrence and deterioration. Clinical tissues, cell and animal models were used to clarify the roles of PLAC8 in CRC tumorigenesis, invasion, and migration. Next-generation sequencing of 16S ribosomal DNA has been used to assess the gut microbiota in stool of CRC patients. We found that PLAC8 was upregulated in tissues from patients with late-stage CRC. In our in vitro studies, PLAC8 was dynamically regulated in mitotic cells. Overexpressed PLAC8 was nucleated at the centrosome during mitosis, and therefore, PLAC8 overexpression might increase cell growth and migration (all p <0.05). The tumorigenic and invasive effects of PLAC8 on CRC cells were also confirmed in a xenograft mouse model. We further identified reduced levels of two butyrate-producing organisms, Butyricicoccus and Prevotella spp., in stools from CRC patients. We found that butyrate downregulated PLAC8 expression and induced apoptosis in PLAC8-overexpressing cells. Our data suggests that PLAC8 gene and protein expression and dysbiosis of gut microflora, especially in butyrate-producing microorganisms, may be indicators of CRC progression.
Original languageTraditional Chinese
JournalJournal of Advanced Research
DOIs
Publication statusPublished - Nov 2019

Cite this

Gut butyrate-producing organisms correlate to Placenta Specific 8 protein: importance to colorectal cancer progression. / Huang, Chi-Cheng; Shen, Ming-Hung; Chen, Shao-Kuan; Yang, Shung-Haur; Liu, Chih-Yi; Guo, Jiun-Wen; Chang, Kang-Wei; Huang, Chi-Jung.

In: Journal of Advanced Research, 11.2019.

Research output: Contribution to journalArticle

Huang, Chi-Cheng ; Shen, Ming-Hung ; Chen, Shao-Kuan ; Yang, Shung-Haur ; Liu, Chih-Yi ; Guo, Jiun-Wen ; Chang, Kang-Wei ; Huang, Chi-Jung. / Gut butyrate-producing organisms correlate to Placenta Specific 8 protein: importance to colorectal cancer progression. In: Journal of Advanced Research. 2019.
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title = "Gut butyrate-producing organisms correlate to Placenta Specific 8 protein: importance to colorectal cancer progression",
abstract = "Tumor metastasis or recurrence often occurs in patients with curative resection of colorectal cancer (CRC). Placental-specific 8 (PLAC8), which has increased expression in stool, may be associated with CRC recurrence. Insights into the role of PLAC8 in CRC recurrence and its clinical significance may support to develop strategies for preventing CRC recurrence and deterioration. Clinical tissues, cell and animal models were used to clarify the roles of PLAC8 in CRC tumorigenesis, invasion, and migration. Next-generation sequencing of 16S ribosomal DNA has been used to assess the gut microbiota in stool of CRC patients. We found that PLAC8 was upregulated in tissues from patients with late-stage CRC. In our in vitro studies, PLAC8 was dynamically regulated in mitotic cells. Overexpressed PLAC8 was nucleated at the centrosome during mitosis, and therefore, PLAC8 overexpression might increase cell growth and migration (all p <0.05). The tumorigenic and invasive effects of PLAC8 on CRC cells were also confirmed in a xenograft mouse model. We further identified reduced levels of two butyrate-producing organisms, Butyricicoccus and Prevotella spp., in stools from CRC patients. We found that butyrate downregulated PLAC8 expression and induced apoptosis in PLAC8-overexpressing cells. Our data suggests that PLAC8 gene and protein expression and dysbiosis of gut microflora, especially in butyrate-producing microorganisms, may be indicators of CRC progression.",
keywords = "Colorectal cancer progression, Gut microbiota, Placenta Specific 8, Butyrate",
author = "Chi-Cheng Huang and Ming-Hung Shen and Shao-Kuan Chen and Shung-Haur Yang and Chih-Yi Liu and Jiun-Wen Guo and Kang-Wei Chang and Chi-Jung Huang",
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journal = "Journal of Advanced Research",
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T1 - Gut butyrate-producing organisms correlate to Placenta Specific 8 protein: importance to colorectal cancer progression

AU - Huang, Chi-Cheng

AU - Shen, Ming-Hung

AU - Chen, Shao-Kuan

AU - Yang, Shung-Haur

AU - Liu, Chih-Yi

AU - Guo, Jiun-Wen

AU - Chang, Kang-Wei

AU - Huang, Chi-Jung

PY - 2019/11

Y1 - 2019/11

N2 - Tumor metastasis or recurrence often occurs in patients with curative resection of colorectal cancer (CRC). Placental-specific 8 (PLAC8), which has increased expression in stool, may be associated with CRC recurrence. Insights into the role of PLAC8 in CRC recurrence and its clinical significance may support to develop strategies for preventing CRC recurrence and deterioration. Clinical tissues, cell and animal models were used to clarify the roles of PLAC8 in CRC tumorigenesis, invasion, and migration. Next-generation sequencing of 16S ribosomal DNA has been used to assess the gut microbiota in stool of CRC patients. We found that PLAC8 was upregulated in tissues from patients with late-stage CRC. In our in vitro studies, PLAC8 was dynamically regulated in mitotic cells. Overexpressed PLAC8 was nucleated at the centrosome during mitosis, and therefore, PLAC8 overexpression might increase cell growth and migration (all p <0.05). The tumorigenic and invasive effects of PLAC8 on CRC cells were also confirmed in a xenograft mouse model. We further identified reduced levels of two butyrate-producing organisms, Butyricicoccus and Prevotella spp., in stools from CRC patients. We found that butyrate downregulated PLAC8 expression and induced apoptosis in PLAC8-overexpressing cells. Our data suggests that PLAC8 gene and protein expression and dysbiosis of gut microflora, especially in butyrate-producing microorganisms, may be indicators of CRC progression.

AB - Tumor metastasis or recurrence often occurs in patients with curative resection of colorectal cancer (CRC). Placental-specific 8 (PLAC8), which has increased expression in stool, may be associated with CRC recurrence. Insights into the role of PLAC8 in CRC recurrence and its clinical significance may support to develop strategies for preventing CRC recurrence and deterioration. Clinical tissues, cell and animal models were used to clarify the roles of PLAC8 in CRC tumorigenesis, invasion, and migration. Next-generation sequencing of 16S ribosomal DNA has been used to assess the gut microbiota in stool of CRC patients. We found that PLAC8 was upregulated in tissues from patients with late-stage CRC. In our in vitro studies, PLAC8 was dynamically regulated in mitotic cells. Overexpressed PLAC8 was nucleated at the centrosome during mitosis, and therefore, PLAC8 overexpression might increase cell growth and migration (all p <0.05). The tumorigenic and invasive effects of PLAC8 on CRC cells were also confirmed in a xenograft mouse model. We further identified reduced levels of two butyrate-producing organisms, Butyricicoccus and Prevotella spp., in stools from CRC patients. We found that butyrate downregulated PLAC8 expression and induced apoptosis in PLAC8-overexpressing cells. Our data suggests that PLAC8 gene and protein expression and dysbiosis of gut microflora, especially in butyrate-producing microorganisms, may be indicators of CRC progression.

KW - Colorectal cancer progression

KW - Gut microbiota

KW - Placenta Specific 8

KW - Butyrate

U2 - 10.1016/j.jare.2019.11.005

DO - 10.1016/j.jare.2019.11.005

M3 - 文章

JO - Journal of Advanced Research

JF - Journal of Advanced Research

SN - 2090-1232

ER -