PMID- 34414111
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20210821
IS  - 2234-943X (Print)
IS  - 2234-943X (Electronic)
IS  - 2234-943X (Linking)
VI  - 11
DP  - 2021
TI  - Acetate Promotes a Differential Energy Metabolic Response in Human HCT 116 and 
      COLO 205 Colon Cancer Cells Impacting Cancer Cell Growth and Invasiveness.
PG  - 697408
LID - 10.3389/fonc.2021.697408 [doi]
LID - 697408
AB  - Under dysbiosis, a gut metabolic disorder, short-chain carboxylic acids (SCCAs) 
      are secreted to the lumen, affecting colorectal cancer (CRC) development. 
      Butyrate and propionate act as CRC growth inhibitors, but they might also serve 
      as carbon source. In turn, the roles of acetate as metabolic fuel and protein 
      acetylation promoter have not been clearly elucidated. To assess whether acetate 
      favors CRC growth through active mitochondrial catabolism, a systematic study 
      evaluating acetate thiokinase (AcK), energy metabolism, cell proliferation, and 
      invasiveness was performed in two CRC cell lines incubated with physiological 
      SCCAs concentrations. In COLO 205, acetate (+glucose) increased the cell density 
      (50%), mitochondrial protein content (3-10 times), 2-OGDH acetylation, and 
      oxidative phosphorylation (OxPhos) flux (36%), whereas glycolysis remained 
      unchanged vs. glucose-cultured cells; the acetate-induced OxPhos activation 
      correlated with a high AcK activity, content, and acetylation (1.5-6-fold). In 
      contrast, acetate showed no effect on HCT116 cell growth, OxPhos, AcK activity, 
      protein content, and acetylation. However, a substantial increment in the HIF-1alpha 
      content, HIF-1alpha-glycolytic protein targets (1-2.3 times), and glycolytic flux 
      (64%) was observed. Butyrate and propionate decreased the growth of both CRC 
      cells by impairing OxPhos flux through mitophagy and mitochondrial fragmentation 
      activation. It is described, for the first time, the role of acetate as metabolic 
      fuel for ATP supply in CRC COLO 205 cells to sustain proliferation, aside from 
      its well-known role as protein epigenetic regulator. The level of AcK determined 
      in COLO 205 cells was similar to that found in human CRC biopsies, showing its 
      potential role as metabolic marker.
CI  - Copyright (c) 2021 Rodriguez-Enriquez, Robledo-Cadena, Gallardo-Perez, 
      Pacheco-Velazquez, Vazquez, Saavedra, Vargas-Navarro, Blanco-Carpintero, 
      Marin-Hernandez, Jasso-Chavez, Encalada, Ruiz-Godoy, Aguilar-Ponce and 
      Moreno-Sanchez.
FAU - Rodriguez-Enriquez, Sara
AU  - Rodriguez-Enriquez S
AD  - Departamento de Bioquimica, Instituto Nacional de Cardiologia, Mexico, Mexico.
FAU - Robledo-Cadena, Diana Xochiquetzal
AU  - Robledo-Cadena DX
AD  - Departamento de Bioquimica, Instituto Nacional de Cardiologia, Mexico, Mexico.
FAU - Gallardo-Perez, Juan Carlos
AU  - Gallardo-Perez JC
AD  - Departamento de Bioquimica, Instituto Nacional de Cardiologia, Mexico, Mexico.
FAU - Pacheco-Velazquez, Silvia Cecilia
AU  - Pacheco-Velazquez SC
AD  - Departamento de Bioquimica, Instituto Nacional de Cardiologia, Mexico, Mexico.
FAU - Vazquez, Citlali
AU  - Vazquez C
AD  - Departamento de Bioquimica, Instituto Nacional de Cardiologia, Mexico, Mexico.
FAU - Saavedra, Emma
AU  - Saavedra E
AD  - Departamento de Bioquimica, Instituto Nacional de Cardiologia, Mexico, Mexico.
FAU - Vargas-Navarro, Jorge Luis
AU  - Vargas-Navarro JL
AD  - Departamento de Bioquimica, Instituto Nacional de Cardiologia, Mexico, Mexico.
FAU - Blanco-Carpintero, Betsy Alejandra
AU  - Blanco-Carpintero BA
AD  - Departamento de Bioquimica, Instituto Nacional de Cardiologia, Mexico, Mexico.
FAU - Marin-Hernandez, Alvaro
AU  - Marin-Hernandez A
AD  - Departamento de Bioquimica, Instituto Nacional de Cardiologia, Mexico, Mexico.
FAU - Jasso-Chavez, Ricardo
AU  - Jasso-Chavez R
AD  - Departamento de Bioquimica, Instituto Nacional de Cardiologia, Mexico, Mexico.
FAU - Encalada, Rusely
AU  - Encalada R
AD  - Departamento de Bioquimica, Instituto Nacional de Cardiologia, Mexico, Mexico.
FAU - Ruiz-Godoy, Luz
AU  - Ruiz-Godoy L
AD  - Banco de Tumores, Instituto Nacional de Cancerologia, Mexico, Mexico.
FAU - Aguilar-Ponce, Jose Luis
AU  - Aguilar-Ponce JL
AD  - Departamento de Medicina Interna, Instituto Nacional de Cancerologia, Mexico, 
      Mexico.
FAU - Moreno-Sanchez, Rafael
AU  - Moreno-Sanchez R
AD  - Departamento de Bioquimica, Instituto Nacional de Cardiologia, Mexico, Mexico.
LA  - eng
PT  - Journal Article
DEP - 20210803
PL  - Switzerland
TA  - Front Oncol
JT  - Frontiers in oncology
JID - 101568867
PMC - PMC8370060
OTO - NOTNLM
OT  - acetate thiokinase
OT  - acetylation
OT  - cancer biomarker
OT  - colon cancer
OT  - oxidative phoshorylation
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2021/08/21 06:00
MHDA- 2021/08/21 06:01
PMCR- 2021/01/01
CRDT- 2021/08/20 07:06
PHST- 2021/04/19 00:00 [received]
PHST- 2021/07/15 00:00 [accepted]
PHST- 2021/08/20 07:06 [entrez]
PHST- 2021/08/21 06:00 [pubmed]
PHST- 2021/08/21 06:01 [medline]
PHST- 2021/01/01 00:00 [pmc-release]
AID - 10.3389/fonc.2021.697408 [doi]
PST - epublish
SO  - Front Oncol. 2021 Aug 3;11:697408. doi: 10.3389/fonc.2021.697408. eCollection 
      2021.