The emerging role of glycolysis and immune evasion in gastric cancer DOI Creative Commons
Shanshan Zheng, Huai Li, Yaqi Li

et al.

Cancer Cell International, Journal Year: 2023, Volume and Issue: 23(1)

Published: Dec. 9, 2023

Abstract Gastric cancer (GC) is the fifth most common malignancy and third leading cause of cancer-related deaths worldwide. Similar to other types tumors, GC cells undergo metabolic reprogramming switch a “predominantly glycolytic” pattern promote its survival metastasis, also known as “the Warburg effect”, which characterized by enhanced glucose uptake lactate production. A large number studies have shown that targeting glycolysis promising strategy, can make more susceptible conventional treatment methods treatment, including chemotherapy, radiotherapy immunotherapy, so on. Therefore, this review summarizes characteristics in focuses on how abnormal concentration lead immunosuppression through effects differentiation, metabolism, function infiltrating immune cells, phenomenon may be potential strategy improve therapeutic efficacy GC.

Language: Английский

<p>Metabolic reprogramming results in abnormal glycolysis in gastric cancer: a review</p> DOI Open Access
Yuanda Liu, Ze Zhang, Junyang Wang

et al.

OncoTargets and Therapy, Journal Year: 2019, Volume and Issue: Volume 12, P. 1195 - 1204

Published: Feb. 1, 2019

The Warburg effect in tumor cells involves the uptake of high levels glucose, enhanced glycolysis, and metabolism pyruvate to lactic acid rather than oxidative phos-phorylation generate energy under aerobic conditions. This is closely related occurrence, invasion, metastasis, drug resistance, poor prognosis gastric cancer (GC). Current research has further demonstrated that GC not only mediated by glycolysis pathway, but also includes roles for mitochondria, noncoding RNAs, other proteins do directly regulate metabolism. As a result, changes pathway lead abnormal glucose metabolism, they affect mitochondrial functions, cellular processes such as apoptosis cell cycle regulation, lipids amino acids. In this review, we discuss metabolic reprogramming based on possible link between lipid clarify role mitochondria. We examine recent studies inhibitors GC.

Language: Английский

Citations

89
Glycolysis promotes the progression of pancreatic cancer and reduces cancer cell sensitivity to gemcitabine DOI Open Access
Shangnan Dai, Yunpeng Peng, Yi Zhu

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2019, Volume and Issue: 121, P. 109521 - 109521

Published: Nov. 2, 2019

Previous studies have reported that increased glycolytic activity enhances chemotherapy resistance in some types of malignancies. However, whether glycolysis influences the curative effect gemcitabine (GEM) on pancreatic cancer (PC) cells remains unclear. The aim this study was to investigate status PC and its association with tolerance GEM. Data from Cancer Genome Atlas (TCGA) were used analyze correlation between glycolysis-related gene (GRG) expression progression prognosis. 2-Deoxy-D-glucose (2-DG) applied assess inhibition cell death GEM tolerance. Expression GRGs, such as HK1, GAPDH, PKM2, LDHA, significantly associated prognosis PC. Furthermore, PKLR, LDHA correlated positively progression. Further analysis revealed markedly enhanced following sensitivity notably presence 2-DG. Our findings indicate abnormally promotes development drug 2-DG combined is a potential therapy for

Language: Английский

Citations

81
CircAKT3 inhibits glycolysis balance in lung cancer cells by regulating miR-516b-5p/STAT3 to inhibit cisplatin sensitivity DOI

Yangling Xu,

Tiantian Jiang,

Changgang Wu

et al.

Biotechnology Letters, Journal Year: 2020, Volume and Issue: 42(7), P. 1123 - 1135

Published: March 13, 2020

Language: Английский

Citations

72
N6-methyladenosine-mediated LDHA induction potentiates chemoresistance of colorectal cancer cells through metabolic reprogramming DOI Creative Commons
Kun Zhang,

Tao Zhang,

Yuhan Yang

et al.

Theranostics, Journal Year: 2022, Volume and Issue: 12(10), P. 4802 - 4817

Published: Jan. 1, 2022

Background: Chemoresistance to 5-fluorouracil (5-FU) is a major barrier influence the treatment efficiency of colorectal cancer (CRC) patients, while precise molecular mechanisms underlying 5-FU resistance remain be fully elucidated.Methods: The metabolic profiles including ATP generation, glucose consumption, lactate and oxygen consumption rate (OCR) in resistant CRC cells were compared with those their parental cells.Subsequently, series vitro vivo experiments carried out investigate responsible for reprogramming cells.Results: We found that showed increased levels OCR as cells.Further, mRNA N 6 -methyladenosine (m A) methyltransferase-like 3 (METTL3) observed cells.Inhibition or knockdown METTL3 can suppress glycolysis restore chemosensitivity cells.Mechanistically, enhances expression LDHA, which catalyzes conversion pyruvate lactate, trigger resistance.METTL3 increase transcription LDHA via stabilizing hypoxia-inducible factor (HIF-1α), further, also triggers translation methylation its CDS region recruitment YTH domain-containing family protein 1 (YTHDF1).Targeted inhibition METTL3/LDHA axis significantly sensitivity cells. Conclusion:Our study indicates axis-induced metabolism potential therapy target overcome

Language: Английский

Citations

60
Baicalein reverses hypoxia-induced 5-FU resistance in gastric cancer AGS cells through suppression of glycolysis and the PTEN/Akt/HIF-1α signaling pathway DOI Open Access
Fenglin Chen,

Mingkai Zhuang,

Canmei Zhong

et al.

Oncology Reports, Journal Year: 2014, Volume and Issue: 33(1), P. 457 - 463

Published: Oct. 17, 2014

Language: Английский

Citations

91
Monocarboxylate transport inhibition potentiates the cytotoxic effect of 5-fluorouracil in colorectal cancer cells DOI
Ricardo Amorim, Céline Pinheiro, Vera Miranda‐Gonçalves

et al.

Cancer Letters, Journal Year: 2015, Volume and Issue: 365(1), P. 68 - 78

Published: May 25, 2015

Language: Английский

Citations

80
Knockdown of KLF5 suppresses hypoxia-induced resistance to cisplatin in NSCLC cells by regulating HIF-1α-dependent glycolysis through inactivation of the PI3K/Akt/mTOR pathway DOI Creative Commons

Tianxiao Gong,

Liuqing Cui,

Haili Wang

et al.

Journal of Translational Medicine, Journal Year: 2018, Volume and Issue: 16(1)

Published: June 14, 2018

Hypoxia-mediated chemoresistance has been regarded as an important obstacle in the development of cancer treatment. Knockdown krüppel-like factor 5 (KLF5) was reported to inhibit hypoxia-induced cell survival and promote apoptosis non-small lung (NSCLC) cells via direct regulation hypoxia inducible factor-1α (HIF-1α) expression. However, roles KLF5 cisplatin (DDP) resistance its underlying mechanism NSCLC remain be further elucidated. Western blot performed determine protein levels KLF5, P-glycoprotein (P-gp) HIF-1α treated cells. Cell examined by MTT assay. The effect knockdown on glycolysis assessed measuring glucose consumption lactate production. phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target rapamycin (mTOR) pathway analyzed western blot. Hypoxia upregulated expression suppressed DDP cells, demonstrated increased cytotoxic effects reduced P-gp hypoxia. Moreover, inhibited glycolysis, inhibiting HIF-1α-dependent Furthermore, activation PI3K/Akt/mTOR overexpression promoted through pathway. could suppress resistance, may due inhibition inactivation

Language: Английский

Citations

79
Activation of mitochondrial oxidation by PDK2 inhibition reverses cisplatin resistance in head and neck cancer DOI
Jong‐Lyel Roh, Jin Young Park, Eun Hye Kim

et al.

Cancer Letters, Journal Year: 2015, Volume and Issue: 371(1), P. 20 - 29

Published: Nov. 23, 2015

Language: Английский

Citations

75
miRNa signature in small extracellular vesicles and their association with platinum resistance and cancer recurrence in ovarian cancer DOI
Mona Alharbi, Shayna Sharma, Dominic Guanzon

et al.

Nanomedicine Nanotechnology Biology and Medicine, Journal Year: 2020, Volume and Issue: 28, P. 102207 - 102207

Published: April 23, 2020

Language: Английский

Citations

58
<p>The combination of the glycolysis inhibitor 2-DG and sorafenib can be effective against sorafenib-tolerant persister cancer cells</p> DOI Open Access
Li Wang, Qian Yang, Shaoyong Peng

et al.

OncoTargets and Therapy, Journal Year: 2019, Volume and Issue: Volume 12, P. 5359 - 5373

Published: July 1, 2019

Chemotherapy remains a major clinical option for the successful treatment of cancer by eliminating fast-growing populations cells. However, drug resistance causes failure antitumor treatment. Increasing evidence suggests that small subpopulation cells will enter "persister state" under pressure. The persister cell pool constitutes reservoir from which may emerge. Therefore, targeting presents therapeutic opportunity to prevent and impede tumor relapse. RT-qPCR, Western blot, Seahorse, apoptosis assay, clonogenic xenografted mouse model were used this study. We showed similar therapy-resistant state underlies behavior derived sorafenib treatments with reversible, nonmutational mechanisms. Then, we demonstrated upregulated glycolysis, as evidenced higher ECAR, well increased glucose consumption lactate production. A database analysis sorafenib-tolerant exhibited expression glycolytic enzyme hexokinase 2, is closely related poor prognosis in liver cancer. found combined inhibitor 2-DG inhibited colony formation. Consequently, when exposed low concentration sorafenib, they suffered mitochondrial dysfunction but compensatory increases contributes growth proliferation. Finally, combination reduced mice. These findings suggest such can effectively hamper represent promising strategy resistance.

Language: Английский

Citations

56