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Gemella morbillorum Promotes Colorectal Carcinogenesis: LPBDCP-Mediated Invasion Activates Ras Signaling and

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Gemella morbillorum promotes colorectal cancer (CRC) by invading host cells and activating oncogenic pathways. Targeting its invasion protein (LPBDCP) or secreted enzyme (NDPD) may inhibit CRC progression.

Keywords:
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Area of Science:

  • Microbiology
  • Oncology
  • Gastroenterology

Background:

  • Gut microbiota dysbiosis is linked to colorectal cancer (CRC) development.
  • Gemella morbillorum has been identified as a key bacterium associated with CRC.
  • Understanding the mechanisms of G. morbillorum in CRC is crucial for therapeutic strategies.

Purpose of the Study:

  • To elucidate the role and mechanisms of Gemella morbillorum in colorectal cancer tumorigenesis.
  • To identify specific bacterial factors and host interactions involved in CRC promotion.
  • To evaluate potential therapeutic targets for G. morbillorum-associated CRC.

Main Methods:

  • Fecal metagenomic analysis and fluorescence in situ hybridization to identify and quantify G. morbillorum.
  • In vitro and in vivo experiments using CRC cell lines and mouse models to assess oncogenic effects.
  • RNA sequencing, co-immunoprecipitation, and mass spectrometry to identify molecular interactions and pathways.
  • Genetic knockout strategies (LPBDCP, TMEM140, NDPD) to validate therapeutic targets.

Main Results:

  • Gemella morbillorum is significantly enriched in CRC tumor tissues.
  • G. morbillorum invades host cells via LPBDCP-TMEM140 interaction, triggering Ca2+ influx and activating PI3K-AKT-NF-κB and RAF-MEK-ERK pathways.
  • Bacterial secretion of NDPD leads to p53 deacetylation and degradation, promoting cell proliferation and inhibiting apoptosis.
  • Genetic disruption of LPBDCP, TMEM140, or NDPD abrogates the tumor-promoting effects of G. morbillorum.

Conclusions:

  • Gemella morbillorum actively promotes colorectal cancer progression through specific invasion and enzymatic mechanisms.
  • The LPBDCP-TMEM140 interaction and NDPD secretion represent critical pathways in G. morbillorum-driven tumorigenesis.
  • Targeting G. morbillorum's invasion factors or secreted enzymes offers promising therapeutic avenues for CRC intervention.