scholarly journals LncRNA HLA Complex Group 11 Knockdown Alleviates Cisplatin Resistance in Gastric Cancer by Targeting the miR-144-3p/UBE2D1 Axis

2021 ◽  
Vol Volume 13 ◽  
pp. 7543-7557
Author(s):  
Yu Li ◽  
Liqin Wang ◽  
Xiaoyi Xu ◽  
Heng Sun ◽  
Leilei Wu
Keyword(s):  
Gastric Cancer ◽  
Cisplatin Resistance ◽  
Complex Group

scholarly journals Mortalin/glucose-regulated protein 75 promotes the cisplatin-resistance of gastric cancer via regulating anti-oxidation/apoptosis and metabolic reprogramming

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yi Dai ◽  
Fan Li ◽  
Yuwen Jiao ◽  
Guoguang Wang ◽  
Tian Zhan ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cisplatin Resistance ◽  
Meta Analysis ◽  
Acquired Resistance ◽  
Hypoxia Inducible Factor ◽  
Metabolic Reprogramming ◽  
Platinum Resistance ◽  
Related Factor ◽  
Platinum Drug ◽  
Glucose Regulated Protein

AbstractPlatinum drug treatment is one of the most predominant chemotherapeutic strategies for patients with gastric cancer (GC). However, the therapeutic effect is less than satisfactory, largely due to the acquired resistance to platinum drugs. Therefore, a better understanding of the underlying mechanisms can greatly improve the therapeutic efficacy of GC. In this study, we aimed to investigate the chemo-resistance related functions/mechanisms and clinical significance of glucose-regulated protein 75 (GRP75) in GC. Here, our data showed that compared with SGC7901 cells, the expression of GRP75 was markedly higher in cisplatin-resistance cells (SGC7901CR). Knockdown of GRP75 abolished the maintenance of mitochondrial membrane potential (MMP) and inhibited the nuclear factor erythroid-2-related factor 2 (NRF2), phosphatidylinositol 3 kinase/protein kinase B (PI3K/AKT), hypoxia-inducible factor 1α (HIF-1α), and c-myc, which resulted in blocking the activation of their downstream targets. These processes attenuated the anti-oxidation/apoptosis abilities and altered the metabolic reprogramming in SGC7901CR cells, leading to re-sensitizing these cells to cisplatin. However, overexpression of GRP75 in SGC7901 cells caused the opposite effects. A xenografts model confirmed the abovementioned results. In GC patients receiving platinum chemotherapy and a meta-analysis, a high level of GRP75 was positively associated with aggressive characteristics and poor prognosis including but not limited to gastrointestinal cancers, and was an independent predictor for overall survival. Collectively, our study indicated that GRP75 was involved in the cisplatin-resistance of GC and that GRP75 could be a potential therapeutic target for restoring the drug response in platinum-resistance cells and a useful additive prognostic tool in guiding clinical management of GC patients.

miR-21 confers cisplatin resistance in gastric cancer cells by regulating PTEN

Toxicology ◽  
2013 ◽  
Vol 306 ◽  
pp. 162-168 ◽  
Author(s):  
Shou-mei Yang ◽  
Cheng Huang ◽  
Xiao-feng Li ◽  
Ming-zhe Yu ◽  
Yong He ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Gastric Cancer Cells

scholarly journals Exosome-transmitted miR-769-5p confers cisplatin resistance and tumorigenesis in gastric cancer by targeting CASP9 and promoting the ubiquitination degradation of p53

2021 ◽  
Author(s):  
Xinming Jing ◽  
Mengyan Xie ◽  
Kun Ding ◽  
Tingting Xu ◽  
Yuan Fang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Microenvironment ◽  
Cisplatin Resistance ◽  
Biologically Active ◽  
Clinical Prognosis ◽  
Anti Cancer ◽  
Ubiquitin Proteasome ◽  
Proteasome Pathway ◽  
New Treatment ◽  
Apoptosis Related Protein

AbstractCisplatin resistance is the main cause of poor clinical prognosis in patients with gastric cancer (GC). Yet, the exact mechanism of cisplatin resistance remains unclear. Recent studies have suggested that exocrine miRNAs found in the tumor microenvironment participates in tumor metastasis and drug resistance. In this study, we discovered that cisplatin-resistant GC cells communicate with the tumor microenvironment by secreting microvesicles. The biologically active miR-769-5p can be integrated into exosomes and delivered to sensitive cells, thereby spreading cisplatin resistance. Mi769-5p was upregulated in GC tissues and enriched in the serum exosomes of cisplatin-resistant patients. Mechanistically, miR-769-5p promotes cisplatin resistance by targeting CASP9 so as to inhibit the downstream caspase pathway and promote the degradation of the apoptosis-related protein p53 through the ubiquitin-proteasome pathway. Targeting miR-769 with its antagonist to treat cisplatin-resistant GC cells can restore the cisplatin response, confirming that exosomal miR-769-5p can be a key regulator of cisplatin resistance in GC. Therefore, exosomal miR-769-5p derived from drug-resistant cells can be used as a potential therapeutic predictor of anti-tumor chemotherapy to enhance the effect of anti-cancer chemotherapy, which provides a new treatment option for GC.

scholarly journals Helicobacter pylori ‐induced miR‐135b‐5p promotes cisplatin resistance in gastric cancer

2018 ◽  
Vol 33 (1) ◽  
pp. 264-274 ◽  
Author(s):  
Linlin Shao ◽  
Zheng Chen ◽  
Mohammed Soutto ◽  
Shoumin Zhu ◽  
Heng Lu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Cisplatin Resistance

Let-7b attenuates cisplatin resistance and tumor growth in gastric cancer by targeting AURKB

2018 ◽  
Vol 25 (11-12) ◽  
pp. 300-308 ◽  
Author(s):  
Xiao Han ◽  
Jing-Jing Zhang ◽  
Zheng-Quan Han ◽  
Hai-Bin Zhang ◽  
Zi-An Wang
Keyword(s):  
Gastric Cancer ◽  
Tumor Growth ◽  
Cisplatin Resistance
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