MCT4 promotes cell proliferation and invasion of castration-resistant prostate cancer PC-3 cell line

Sun, Qing; Hu, Lan; Fu, Qiang

doi:10.17179/excli2018-1879

Cited by 7 publications

(4 citation statements)

References 26 publications

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“…High expression of this gene has been associated with presence of immunosuppressive cells and factors in lung adenocarcinoma, which might be responsible for microenvironment immunosuppression [ 121 ]. SLC16A3 has been associated cancer proliferation and invasion [ 122 , 123 ], and this gene has been shown to be upregulated in lung adenocarcinoma [ 124 ]. The gene APOE is associated with regulation of lipid metabolism.…”

Section: Resultsmentioning

confidence: 99%

Increased heterogeneity in expression of genes associated with cancer progression and drug resistance

Bose,

Datta,

Mandal

et al. 2024

Translational Oncology

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Section: Resultsmentioning

confidence: 99%

Increased heterogeneity in expression of genes associated with cancer progression and drug resistance

Bose,

Datta,

Mandal

et al. 2024

Translational Oncology

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“…Previous studies have demonstrated that silencing MCT4 in certain tumor cells can reduce the migration and invasion of the cells, but the mechanism by which MCT4 promotes migration is inconsistent in different tumor cell models ( 16 , 21 , 64 , 65 ). For instance, MCT4 is reported to promote tumor cell invasion and migration through the integrin β4-SRC-FAK and MEK-ERK pathways in oral squamous cell carcinoma ( 16 ).…”

Section: Discussionmentioning

confidence: 99%

“…By contrast, MCT4 has been suggested to facilitate the metastasis of renal cancer cells through integrin β1 ( 64 ), while MCT4 has been demonstrated to promote hepatocellular migration via upregulation of the trafficking protein particle complex subunit 5 (TRAPPC5) gene ( 65 ). Furthermore, MCT4 has been shown to promote the invasion of prostate cancer cells via the regulation of invasion-associated genes, including VEGF, CD147, MMP2 and MMP9 ( 21 ). These findings are from studies in which MCT4 was silenced in one type of tumor cell, and the mechanism by which MCT4 promotes migration varies among the different tumor cell models.…”

Section: Discussionmentioning

confidence: 99%

“…In previous studies the knockdown of MCT4 expression was shown to decrease the migration and invasion of lung cancer ( 18 ), oral squamous cell carcinoma ( 16 ), hepatocellular carcinoma ( 19 ), pancreatic ductal adenocarcinoma ( 20 ), prostate cancer ( 21 ), glioma ( 22 ) and breast cancer cells ( 23 ). These studies involved the transient silencing of MCT4 in various types of tumor cells and were mostly limited to describing the decreased migration after MCT4 silencing.…”

Section: Introductionmentioning

confidence: 98%

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Monocarboxylate transporter 4 promotes the migration of non‑cancerous L929 fibroblast cells by activating the IGF1/IGF1R/PIK3R3/SGK1 axis

Zhou,

Wang,

et al. 2023

Oncol Lett

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The tumor microenvironment (TME) and Warburg effect are critical for the regulation of tumor metastasis. The monocarboxylate transporter (MCT) family members, particularly MCT4, which is encoded by the solute carrier family 16 member 3 gene, play an important role in the regulation of the TME and mediation of the Warburg effect by transporting lactate out of cancer cells. Migration and invasion are two key features of metastasis. Few studies have investigated the mechanism by which MCT4 promotes cell migration, and the suggested mechanisms by which MCT4 promotes migration vary in different tumor cell models. The purpose of the present study was to use non-cancerous cells as a research model to investigate the specific mechanism underlying the promotion of migration by MCT4. In a previous study, murine L929 cells overexpressing human MCT4 (MCT4-L929 cells) were generated and MCT4 was demonstrated to promote the migration and invasion of these non-cancerous cells. In the present study, MCT4-L929 cells and control-L929 cells were used to investigate the potential pathways and mechanisms through which MCT4 promotes cell migration. RNA sequencing analysis revealed 872 differentially expressed genes, comprising 337 and 535 upregulated and downregulated genes, respectively, in the MCT4-L929 cells. Reverse transcription-quantitative analysis and western blotting revealed that MCT4 overexpression increased the transcription and protein levels of insulin-like growth factor 1 (IGF1). In a wound healing assay, the migration of exogenous mouse IGF1-treated control-L929 cells was similar to that of MCT4-L929 cells. Additionally, the inhibition of IGF1 receptor (IGF1R) or serum/glucocorticoid regulated kinase 1 (SGK1), a downstream protein in the IGF1 and phosphoinositide 3-kinase PI3K regulatory subunit 3 (PIK3R3) pathways, in MCT4-L929 cells mitigated the cell migration-promoting effect of MCT4. These novel findings suggest that MCT4 may promote the migration of L929 fibroblast cells via activation of the IGF1/IGF1R/PIK3R3/SGK1 axis.

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Metabolic reprograming of MDSCs within tumor microenvironment and targeting for cancer immunotherapy

Xiang

2021

Acta Pharmacol Sin

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MCT4 promotes cell proliferation and invasion of castration-resistant prostate cancer PC-3 cell line

Cited by 7 publications

References 26 publications

Increased heterogeneity in expression of genes associated with cancer progression and drug resistance

Increased heterogeneity in expression of genes associated with cancer progression and drug resistance

Monocarboxylate transporter 4 promotes the migration of non‑cancerous L929 fibroblast cells by activating the IGF1/IGF1R/PIK3R3/SGK1 axis

Metabolic reprograming of MDSCs within tumor microenvironment and targeting for cancer immunotherapy

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