Facing Cell Autophagy in Gastric Cancer – What Do We Know so Far?

Xiu, Ting; Guo, Qie; Jing, Fanbo

doi:10.2147/ijgm.s298705

Cited by 6 publications

(7 citation statements)

References 136 publications

(135 reference statements)

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“…Based on The Cancer Genome Atlas database, gene expression data for GC patients undergoing numerous other molecular markers have been recognized to possess prognostic value and their expression patterns of autophagy-related genes (ATGs) in GC cells, which served as a hallmark of autophagy regulation (Liu et al, 2021b). Autophagy and GC are controlled by crucial kinases such as mTOR, PI3K/AKT, AMPK, and MAPK, as well as epidermal growth factor receptor, cell cycle mediators, vascular endothelial growth factor, cytokines, apoptosis-associated regulators, and miRNAs (Xiu et al, 2021). ATG5 has been found to participate in autophagosome elongation as a vital regulator and is crucial for autophagy, which is associated with chemotherapy resistance of maximum cancer cells (Wang et al, 2019).…”

Section: Autophagy Markers Expressed In Gc Progressionmentioning

confidence: 99%

“…Furthermore, autophagy regulates in the activation of several cancer-related genes, which inhibits tumor promotion and suppression (Botti et al, 2006;Maiuri et al, 2009). Recent studies have widely explained the involvement of autophagy in GC growth, metastasis, and forecasting (Xu et al, 2020a;Spirina et al, 2020;Xiu et al, 2021). Moreover, microRNAs (miRNAs), short (~22 nucleotides in length) noncoding RNA molecules, can control gene expression at a posttranscriptional level, which has an important association in autophagy-mediated GC regulation.…”

Section: Introductionmentioning

confidence: 99%

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Potential Therapeutic Action of Autophagy in Gastric Cancer Managements: Novel Treatment Strategies and Pharmacological Interventions

et al. 2022

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Gastric cancer (GC), second most leading cause of cancer-associated mortality globally, is the cancer of gastrointestinal tract in which malignant cells form in lining of the stomach, resulting in indigestion, pain, and stomach discomfort. Autophagy is an intracellular system in which misfolded, aggregated, and damaged proteins, as well as organelles, are degraded by the lysosomal pathway, and avoiding abnormal accumulation of huge quantities of harmful cellular constituents. However, the exact molecular mechanism of autophagy-mediated GC management has not been clearly elucidated. Here, we emphasized the role of autophagy in the modulation and development of GC transformation in addition to underlying the molecular mechanisms of autophagy-mediated regulation of GC. Accumulating evidences have revealed that targeting autophagy by small molecule activators or inhibitors has become one of the greatest auspicious approaches for GC managements. Particularly, it has been verified that phytochemicals play an important role in treatment as well as prevention of GC. However, use of combination therapies of autophagy modulators in order to overcome the drug resistance through GC treatment will provide novel opportunities to develop promising GC therapeutic approaches. In addition, investigations of the pathophysiological mechanism of GC with potential challenges are urgently needed, as well as limitations of the modulation of autophagy-mediated therapeutic strategies. Therefore, in this review, we would like to deliver an existing standard molecular treatment strategy focusing on the relationship between chemotherapeutic drugs and autophagy, which will help to improve the current treatments of GC patients.

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Section: Autophagy Markers Expressed In Gc Progressionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Potential Therapeutic Action of Autophagy in Gastric Cancer Managements: Novel Treatment Strategies and Pharmacological Interventions

et al. 2022

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“…Many studies have reported that specimens with gastric malignancy present less expression of miR-1265 than normal tissues. MiR-1265 binds in the region of the gene that encodes calcium-binding protein 39 (CAB39), a key protein for the formation of CAB39-LKB1-STRAD complex, in the Thr172 site of their junction [44]. The CAB39-LKB1-STRAD complex normally influences the phosphorylation of the AMPK signaling pathway, which presents a 100-fold increase [45].…”

Section: Regulation Of Autophagy By Mirnas As Tumor Suppressor Genesmentioning

confidence: 99%

“…Another non-coding RNA is miR-495-3p, which contributes to the inhibition of autophagy-promoted gastric carcinogenesis, as well as to the conversion of multi-drugresistant (MDR) cases of GC, via the downregulation of mTOR pathway, while the limited action of miR-495-3p enhances the malignant phenotype [44]. The same role, as downregulators of the mTOR signaling pathway for autophagy are miR-21 [47], miR-361-5p [48], and miR-375 [44]. Decreased progression and multiplication of gastric cancer cell lines are associated with the expression of other miRNAs such as miR-532-3p, miR-181a, miR-133a-3p, miR-30a, and miR-1et-7a [44].…”

Section: Regulation Of Autophagy By Mirnas As Tumor Suppressor Genesmentioning

confidence: 99%

“…The same role, as downregulators of the mTOR signaling pathway for autophagy are miR-21 [47], miR-361-5p [48], and miR-375 [44]. Decreased progression and multiplication of gastric cancer cell lines are associated with the expression of other miRNAs such as miR-532-3p, miR-181a, miR-133a-3p, miR-30a, and miR-1et-7a [44].…”

Section: Regulation Of Autophagy By Mirnas As Tumor Suppressor Genesmentioning

confidence: 99%

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The Implication of Autophagy in Gastric Cancer Progression

Koustas

Trifylli

Sarantis

et al. 2021

Life

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Gastric cancer is the fifth most common malignancy and the third leading cause of cancer-related death worldwide. The three entirely variable entities have distinct epidemiology, molecular characteristics, prognosis, and strategies for clinical management. However, many gastric tumors appear to be resistant to current chemotherapeutic agents. Moreover, a significant number of gastric cancer patients, with a lack of optimal treatment strategies, have reduced survival. In recent years, multiple research data have highlighted the importance of autophagy, an essential catabolic process of cytoplasmic component digestion, in cancer. The role of autophagy as a tumor suppressor or tumor promoter mechanism remains controversial. The multistep nature of the autophagy process offers a wide array of targetable points for designing novel chemotherapeutic strategies. The purpose of this review is to summarize the current knowledge regarding the interplay between gastric cancer development and the autophagy process and decipher the role of autophagy in this kind of cancer. A plethora of different agents that direct or indirect target autophagy may be a novel therapeutic approach for gastric cancer patients.

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