PMID- 27127175
OWN - NLM
STAT- MEDLINE
DCOM- 20171226
LR  - 20220317
IS  - 1949-2553 (Electronic)
IS  - 1949-2553 (Linking)
VI  - 7
IP  - 22
DP  - 2016 May 31
TI  - Monocarboxylate transporter 1 contributes to growth factor-induced tumor cell 
      migration independent of transporter activity.
PG  - 32695-706
LID - 10.18632/oncotarget.9016 [doi]
AB  - Tumor progression to metastatic disease contributes to the vast majority of 
      incurable cancer. Understanding the processes leading to advanced stage cancer is 
      important for the development of future therapeutic strategies. Here, we 
      establish a connection between tumor cell migration, a prerequisite to 
      metastasis, and monocarboxylate transporter 1 (MCT1). MCT1 transporter activity 
      is known to regulate aspects of tumor progression and, as such, is a clinically 
      relevant target for treating cancer. Knockdown of MCT1 expression caused 
      decreased hepatocyte growth factor (HGF)-induced as well as epidermal growth 
      factor (EGF)-induced tumor cell scattering and wound healing. Western blot 
      analysis suggested that MCT1 knockdown (KD) hinders signaling through the HGF 
      receptor (c-Met) but not the EGF receptor. Exogenous, membrane-permeable MCT1 
      substrates were not able to rescue motility in MCT1 KD cells, nor was 
      pharmacologic inhibition of MCT1 able to recapitulate decreased cell motility as 
      seen with MCT1 KD cells, indicating transporter activity of MCT1 was dispensable 
      for EGF- and HGF-induced motility. These results indicate MCT1 expression, 
      independent of transporter activity, is required for growth factor-induced tumor 
      cell motility. The findings presented herein suggest a novel function for MCT1 in 
      tumor progression independent of its role as a monocarboxylate transporter.
FAU - Gray, Alana L
AU  - Gray AL
AD  - Louisiana State University Health Sciences Center-Shreveport, Shreveport, LA, 
      USA.
AD  - Feist-Weiller Cancer Center, Shreveport, LA, USA.
FAU - Coleman, David T
AU  - Coleman DT
AD  - Louisiana State University Health Sciences Center-Shreveport, Shreveport, LA, 
      USA.
AD  - Feist-Weiller Cancer Center, Shreveport, LA, USA.
FAU - Shi, Runhua
AU  - Shi R
AD  - Louisiana State University Health Sciences Center-Shreveport, Shreveport, LA, 
      USA.
AD  - Feist-Weiller Cancer Center, Shreveport, LA, USA.
FAU - Cardelli, James A
AU  - Cardelli JA
AD  - Louisiana State University Health Sciences Center-Shreveport, Shreveport, LA, 
      USA.
AD  - Feist-Weiller Cancer Center, Shreveport, LA, USA.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Oncotarget
JT  - Oncotarget
JID - 101532965
RN  - 0 (Monocarboxylic Acid Transporters)
RN  - 0 (Muscle Proteins)
RN  - 0 (SLC16A4 protein, human)
RN  - 0 (Symporters)
RN  - 0 (monocarboxylate transport protein 1)
RN  - 33X04XA5AT (Lactic Acid)
RN  - 62229-50-9 (Epidermal Growth Factor)
RN  - 67256-21-7 (Hepatocyte Growth Factor)
RN  - EC 2.7.10.1 (MET protein, human)
RN  - EC 2.7.10.1 (Proto-Oncogene Proteins c-met)
SB  - IM
MH  - Cell Line, Tumor
MH  - Cell Movement/*drug effects
MH  - Epidermal Growth Factor/*pharmacology
MH  - Gene Expression Regulation, Neoplastic
MH  - Hepatocyte Growth Factor/*pharmacology
MH  - Humans
MH  - Lactic Acid/metabolism
MH  - Monocarboxylic Acid Transporters/genetics/*metabolism
MH  - Muscle Proteins/genetics/metabolism
MH  - Neoplasm Invasiveness
MH  - Phosphorylation
MH  - Proto-Oncogene Proteins c-met/metabolism
MH  - RNA Interference
MH  - Signal Transduction
MH  - Symporters/genetics/*metabolism
MH  - Time Factors
MH  - Transfection
PMC - PMC5078044
OTO - NOTNLM
OT  - EGF
OT  - HGF
OT  - MCT1
OT  - cancer
OT  - motility
COIS- The authors have no relevant conflicts of interest to disclose.
EDAT- 2016/04/30 06:00
MHDA- 2017/12/27 06:00
PMCR- 2016/05/31
CRDT- 2016/04/30 06:00
PHST- 2016/01/26 00:00 [received]
PHST- 2016/03/31 00:00 [accepted]
PHST- 2016/04/30 06:00 [entrez]
PHST- 2016/04/30 06:00 [pubmed]
PHST- 2017/12/27 06:00 [medline]
PHST- 2016/05/31 00:00 [pmc-release]
AID - 9016 [pii]
AID - 10.18632/oncotarget.9016 [doi]
PST - ppublish
SO  - Oncotarget. 2016 May 31;7(22):32695-706. doi: 10.18632/oncotarget.9016.