Ghrelin Affects Gastric Cancer Progression by Activating AMPK Signaling Pathway

Hu, Xiaolin; Zhu, Yongjun; Hu, Changhua; Li, You; Wu, Juan; He, Xiaoyan; Huang, Wenjie; Wu, Zonghui

doi:10.1007/s10528-020-10022-x

Cited by 9 publications

(12 citation statements)

References 48 publications

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“…Also, GHRL expression was not associated with GC stages. This result agreed with Pritchett et al, 2020 and Hu et al, 2021 [21], [22].…”

Section: Discussionsupporting

confidence: 92%

“…Also, AMPK is a negative regulator of Warburg effect to suppress of GC development [27]. Recent study by Hu et al 2021 [22] recognized that overexpression of GHRL inhibited GC cell proliferation, invasion, and supported apoptosis by activating AMPK pathway. GHRL knockdown enhanced uptake of glucose and release of lactic acid, indicating that GHRL provoked the anti-Warburg effect through AMPK signaling pathway to prevent GC.…”

Section: Discussionmentioning

confidence: 99%

“…LncRNA GHRLOS has been recognized as the overlapping gene on GHRL antisense strand and can serve as a suppressor of its overlapping gene [28]. Interestingly, it has been proven that ghrelin-AMPK signaling utilizes the anti-Warburg effect to inhibit GC progress [22]. Regarding lncRNA GHRLOS, previous study suggested that lncRNA GHRLOS can play role in the regulation of glyco-metabolism [29].…”

Section: Discussionmentioning

confidence: 99%

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Gene Profiling of SEC13, SMAD7, GHRL, Long Non-Coding RNA GHRLOS, HIF-1α In Gastric Cancer Patients

Hussein

Rashad

Ibrahim

et al. 2022

Preprint

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Background: Even with considerable progress in cancer researches, gastric cancer is still one of the global health problems. Recognition of the differential expressed genes in GC is the most appropriate approach for establishing new diagnostic targets. This study evaluates SEC13, SMAD7, GHRL, lncRNA GHRLOS, HIF-1α genes profiling as well as HIF-1α protein level for GC.Methods: The expression of selected genes, serum HIF-1α and CEA protein levels were determined for 50 GC patients and 50 healthy controls by real-time RT-PCR, ELISA, and ELICA respectively. The sensitivities of these parameters as diagnostic biomarkers were evaluated.Results: SMAD7, HIF-1α expression, serum HIF-1α, and CEA level were significantly upregulated in GC patients as compared to the control group and had significant positive correlations between most of them. On the other hand, SEC13, GHRL, and LncRNA GHRLOS expression were significantly downregulated in GC patients and had significant positive correlations with each other. Significant negative correlations were observed between most of both groups. All studied parameters were associated with GC clinical stages except SMAD7 was associated with stage IV only and GHRL did not associate with tumor stages.Conclusions: All studied parameters may be promising biomarkers for the early diagnosis of GC. SMAD7, HIF-1α gene, and HIF-1α protein may be jointly implicated in cancer development and prognosis, while SEC13, GHRL, and lncRNA GHRLOS may act as tumor suppressors.

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“…Also, GHRL expression was not associated with GC stages. This result agreed with Pritchett et al, 2020 and Hu et al, 2021 [21], [22].…”

Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Gene Profiling of SEC13, SMAD7, GHRL, Long Non-Coding RNA GHRLOS, HIF-1α In Gastric Cancer Patients

Hussein

Rashad

Ibrahim

et al. 2022

Preprint

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“…In contrast to the abovementioned reports, there are also studies showing that ghrelin may inhibit cancer cell proliferation. Ghrelin-induced inhibitory effects on cell proliferation were observed, among others, in human gastric carcinoma cell line AGS [ 246 ]; in N-PAP and ARO thyroid carcinoma cell lines [ 247 ]; in human breast carcinoma cell lines (MCF7, T47D, and MDA-MB231) [ 248 ]; in ovarian cancer cell line HO-8910 [ 249 , 250 ]; and in human prostate carcinoma PC-3 cells [ 251 ].…”

Section: Ghrelin and Cancermentioning

confidence: 99%

“…On the other hand, there are studies showing that ghrelin exhibits anticancer effects. For example, Hu et al [ 246 ] found that overexpression of ghrelin inhibits gastric cancer cell proliferation, cell migration, invasion, and promotes apoptosis. Those effects are associated with the activation of the AMPK pathway, while treatment with D-[lys3]-GHRP-6, a ghrelin receptor antagonist, reverses these effects, promoting tumorigenesis.…”

Section: Ghrelin and Cancermentioning

confidence: 99%

Protective and Healing Effects of Ghrelin and Risk of Cancer in the Digestive System

Ginter

Ceranowicz

Warzecha

2021

IJMS

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Ghrelin is an endogenous ligand for the ghrelin receptor, previously known as the growth hormone secretagogue receptor. This hormone is mainly produced by endocrine cells present in the gastric mucosa. The ghrelin-producing cells are also present in other organs of the body, mainly in the digestive system, but in much smaller amount. Ghrelin exhibits a broad spectrum of physiological effects, such as stimulation of growth hormone secretion, gastric secretion, gastrointestinal motility, and food intake, as well as regulation of glucose homeostasis and bone formation, and inhibition of inflammatory processes. This review summarizes the recent findings concerning animal and human data showing protective and therapeutic effects of ghrelin in the gut, and also presents the role of growth hormone and insulin-like growth factor-1 in these effects. In addition, the current data on the possible influence of ghrelin on the carcinogenesis, its importance in predicting the risk of developing gastrointestinal malignances, as well as the potential usefulness of ghrelin in the treatment of cancer, have been presented.

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Circulating hormones and risk of gastric cancer by subsite in three cohort studies

et al. 2023

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Background Obesity has been positively associated with gastric cancer. Excess fat impacts hormones, which have been implicated in carcinogenesis. We investigated obesity-related hormones and cardia gastric cancer (CGC) and non-cardia gastric cancer (NCGC) risk. Methods Nested case–control studies were conducted within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort (61 CGCs, and 172 NCGCs and matched controls) and the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) study (100 CGCs and 65 NCGCs and matched controls); serum hormones were measured. In UK-Biobank (n = 458,713), we included 137 CGCs and 92 NCGCs. Sex-specific analyses were conducted. For EPIC and ATBC, odds ratios (ORs), and for UK-Biobank hazard ratios (HRs), were estimated using conditional logistic regression and Cox regression, respectively. Results Insulin-like growth-factor-1 was positively associated with CGC and NCGC in EPIC men (ORper 1-SD increase 1.94, 95% CI 1.03–3.63; ORper 1-SD increase 1.63, 95% CI 1.05–2.53, respectively), with similar findings for CGC in UK-Biobank women (HRper 1-SD increase 1.76, 95% CI 1.08–2.88). Leptin in EPIC men and C-peptide in EPIC women were positively associated with NCGC (ORT3 vs. T1 2.72, 95% CI 1.01–7.34 and ORper 1-SD increase 2.17, 95% CI 1.19–3.97, respectively). Sex hormone-binding globulin was positively associated with CGC in UK-Biobank men (HRper 1-SD increase 1.29, 95% CI 1.02–1.64). Conversely, ghrelin was inversely associated with NCGC among EPIC and ATBC men (ORper 1-SD increase 0.53, 95% CI 0.34–0.84; ORper 1-SD increase 0.22, 95% CI 0.10–0.50, respectively). In addition, dehydroepiandrosterone was inversely associated with CGC in EPIC and ATBC men combined. Conclusions Some obesity-related hormones influence CGC and NCGC risk.

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Ghrelin Affects Gastric Cancer Progression by Activating AMPK Signaling Pathway

Cited by 9 publications

References 48 publications

Gene Profiling of SEC13, SMAD7, GHRL, Long Non-Coding RNA GHRLOS, HIF-1α In Gastric Cancer Patients

Gene Profiling of SEC13, SMAD7, GHRL, Long Non-Coding RNA GHRLOS, HIF-1α In Gastric Cancer Patients

Protective and Healing Effects of Ghrelin and Risk of Cancer in the Digestive System

Circulating hormones and risk of gastric cancer by subsite in three cohort studies

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