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October 13, 2021Cancer ResearchOpen Access

ANGPTL4-Mediated Promotion of Glycolysis Facilitates the Colonization of Fusobacterium nucleatum in Colorectal Cancer

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Why the study?

Although Fusobacterium nucleatum contributes to colorectal cancer development, metastasis, and chemoresistance, the mechanisms underlying its colonization in colorectal cancer tissue remain unclear.

Population

Colorectal cancer cells in vitro and in vivo, and patient tumors

Comparison

Fusobacterium nucleatum infection vs uninfected controls

Design

In vitro and in vivo preclinical study

Discussion

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Overview

ANGPTL4 may be a target in F. nucleatum-associated colorectal cancer; animal data leave clinical translation open.

Structured PICO

P
Population
Human colorectal cancer cell lines (DLD1, SW480, HCT-116, HT-29), normal human colon mucosal epithelial cell line NCM460, male 4-week-old BALB/c nude mice xenograft models, TCGA-COAD cohort (n=469 solid tumors, 41 normal tissues), and paraffin-embedded colon adenocarcinoma tissues (n=27).
I
Intervention
F. nucleatum infection, ANGPTL4 overexpression/knockdown, and 2-deoxy-D-glucose (2DG) treatment.
C
Comparator
Uninfected cells, vehicle treatment, and non-target shRNA control.
O
Outcome
F. nucleatum colonization, glycolysis activity (ECAR), ANGPTL4 expression, and tumor volume.surrogate

F. nucleatum colonization in colorectal cancer is regulated by ANGPTL4-mediated glycolysis, providing a potential target for combined repression of F. nucleatum and cancer progression.

Cite This Study

A 2021 study studied this question.

synapsesocial.com/papers/6a7e33024928f3552d3c3766https://doi.org/10.1158/0008-5472.can-21-2273
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