SLC6A14 promotes cell migration and inhibits autophagy in gastric cancer by regulating JAK2/STAT3 signaling

Wang, Haifeng; Wang, Jindao

doi:10.4314/tjpr.v21i6.6

Cited by 3 publications

(3 citation statements)

References 14 publications

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“…Surgical procedures are the only treatment strategy for GC. However, most GC patients' conditions have deteriorated and are at an advanced stage at initial diagnosis, and thus miss the optimal opportunity for surgery [13]. Chemotherapy, radiotherapy and targeted therapy show a relatively high response for advanced GC [14].…”

Section: Discussionmentioning

confidence: 99%

E2F6 promotes cell proliferation and invasion in gastric cancer through the regulation of lncRNA TUSC7

Huang¹,

Qiao²,

Zheng³

et al. 2023

Trop. J. Pharm Res

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Purpose: To examine the regulatory effects of E2F6/long noncoding ribonucleic acid (lncRNA) TUSC7 on the progression of gastric cancer (GC), and the underlying mechanism of action. Methods: Relative levels of E2F6 and TUSC7 in GC tissues were determined by quantitative real-time polymerase chain reaction (qRT-PCR). The influence of TUSC7 on the overall survival of patients with GC was analyzed using Kaplan-Meier method. Interaction between E2F6 and TUSC7 was analyzed by Spearman correlation test and dual-luciferase reporter gene assay. Changes in proliferation, invasion and apoptosis of BGC823 and SGC7901 cells regulated by E2F6 and TUSC7 were assessed. The protein levels of MMP-2 and the activity of caspase-3 were evaluated in GC cells treated with E2F6 and TUSC7 using western blot and caspase-3 kit. Results: TUSC7 was downregulated while E2F6 was upregulated in GC tissues and cells. A negative correlation was observed between the expression levels of TUSC7 and E2F6, and a low level of TUSC7 predicted poor prognosis in GC patients. The knockdown of E2F6 attenuated cell viability and invasion, and stimulated the apoptosis of GC cells, but these were reversed by co-knockdown of TUSC7. In addition, knockdown of E2F6 downregulated MMP-2 protein levels, and upregulated caspase-3 GC cells, but these changes were partially reversed by co-transfection of si-TUSC7. Conclusion: TSUC7 is downregulated in GC, and its low level predicts poor prognosis in GC patients. E2F6 promotes proliferation and invasion of GC cells by negatively regulating TUSC7. Therefore, E2F6/TUSC7 may be utilized as potential therapeutic targets for GC.

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Section: Discussionmentioning

confidence: 99%

E2F6 promotes cell proliferation and invasion in gastric cancer through the regulation of lncRNA TUSC7

Huang¹,

Qiao²,

Zheng³

et al. 2023

Trop. J. Pharm Res

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“…For example, it can help tumor cells take up methionine to maintain DNA methylation and mediate the transport of carnitine ( Nakanishi et al, 2001 ; Sniegowski et al, 2021 ). SLC6A14 is overexpressed in colorectal cancer ( Lu et al, 2022 ), ER + breast cancer ( Karunakaran et al, 2011 ), gastric cancer ( Wang and Wang, 2022 ), pancreatic cancer ( Schniers et al, 2022 ), and cervical cancer ( Sikder et al, 2018 ), closely related to lower overall survival. α-Methyltryptophan (α-MT), a pharmacological inhibitor of SLC6A14, can inhibit the proliferation of cancer cells in vitro and tumor growth in vivo ( Karunakaran et al, 2011 ; Coothankandaswamy et al, 2016 ; Lu et al, 2022 ).…”

Section: Drugs Targeting Glutamine Metabolism For Cancer Treatmentmentioning

confidence: 99%

Exploiting the Achilles’ heel of cancer: disrupting glutamine metabolism for effective cancer treatment

Fan,

Xue,

et al. 2024

Front. Pharmacol.

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Cancer cells have adapted to rapid tumor growth and evade immune attack by reprogramming their metabolic pathways. Glutamine is an important nitrogen resource for synthesizing amino acids and nucleotides and an important carbon source in the tricarboxylic acid (TCA) cycle and lipid biosynthesis pathway. In this review, we summarize the significant role of glutamine metabolism in tumor development and highlight the vulnerabilities of targeting glutamine metabolism for effective therapy. In particular, we review the reported drugs targeting glutaminase and glutamine uptake for efficient cancer treatment. Moreover, we discuss the current clinical test about targeting glutamine metabolism and the prospective direction of drug development.

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“…Gastric cancer (GC) is a prevalent malignancy affecting the digestive tract. Despite significant advancements in treatment, the primary cause of high mortality rates is the metastasis and recurrence of advanced gastric cancer [1]. Therefore, it is of great significance to explore new diagnostic markers and therapeutic targets for the treatment and prognosis of gastric cancer.…”

Section: Introductionmentioning

confidence: 99%

CircRTN4 inhibits the progression of gastric cancer by sponging miR-424-5p and regulating LATS2 expression

Li¹,

Wang²,

Chen³

et al. 2023

Trop. J. Pharm Res

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Purpose: To determine the expression of circRTN4 in gastric cancer (GC) and its role in tumor progression. Methods: GEO dataset GSE93541 was analyzed using GEO2R. Starbase website was used to predict the combination of miRNA and circRTN4. The relationship between circRTN4 and prognosis was analyzed using Kaplan-Meier Plotter database, while expression levels of circRTN4, miR-424-5p, and LATS2 were assessed by quantitative real time-polymerase chain reaction (qRT-PCR). CCK8, EDU, Transwell, and Western blot were used to assess GC proliferation, migration, invasion, and stemness. Lastly, co-transfection of miR-424-5p or si-LAST2 was reversely used to demonstrate the regulatory effect of circRTN4 on the progression of gastric cancer cells. Significantly downregulated circRTN4 in GC was screened, and the combined miR-424-5p and downstream gene LATS2 were predicted by Starbase. Results: The average relative expression of circRTN4 mRNA in GC tissues was significantly lower than in adjacent tissues. MiR-424-5p was highly expressed in tumor tissues, while LATS2 decreased (p < 0.05). Low expression of circRTN4 was associated with a low survival rate in patients. pLCDH- circRTN4 significantly inhibited the proliferation of gastric cancer cells (p < 0.05). Overexpression of circRTN4 inhibited the migration and invasion of tumor cells, while pLCDH-circRTN4 reduced the ability of GC stem cells and expressions of MMP2 and OCT4. Conclusion: Expression of circRTN4 decreases in GC, and contributes to the development and progression of this disease by increasing the levels of LATS2 and binding with miR-424-5p. This suggests that circRTN4 may serve as a promising prognostic marker as well as a potential therapeutic target for gastric cancer

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SLC6A14 promotes cell migration and inhibits autophagy in gastric cancer by regulating JAK2/STAT3 signaling

Cited by 3 publications

References 14 publications

E2F6 promotes cell proliferation and invasion in gastric cancer through the regulation of lncRNA TUSC7

E2F6 promotes cell proliferation and invasion in gastric cancer through the regulation of lncRNA TUSC7

Exploiting the Achilles’ heel of cancer: disrupting glutamine metabolism for effective cancer treatment

CircRTN4 inhibits the progression of gastric cancer by sponging miR-424-5p and regulating LATS2 expression

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