1,25-Dihydroxyvitamin D3 and cisplatin synergistically induce apoptosis and cell cycle arrest in gastric cancer cells

Bao, Anyu; Li, Yan; Zheng, Hongyun; Wu, Wei; Wei, Chuandong

doi:10.3892/ijmm.2014.1664

Cited by 37 publications

(30 citation statements)

References 40 publications

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“…The ability of 1,25(OH) 2 D 3 to induce growth arrest has been widely studied in cancer cells, such as ovarian, prostate, breast, and gastric cancer cells [36][37][38][39], but this is the first report of this effect in human preadipocytes.…”

Section: Discussionmentioning

confidence: 98%

Role of 1α,25-Dihydroxyvitamin D3 in Adipogenesis of SGBS Cells: New Insights into Human Preadipocyte Proliferation

Felicidade¹,

Sartori

Coort

et al. 2018

Cell Physiol Biochem

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Background/Aims: Compared with non-obese individuals, obese individuals commonly store more vitamin D in adipose tissue. VDR expression in adipose tissue can influence adipogenesis and is therefore a target pathway deserving further study. This study aims to assess the role of 1,25(OH)₂D₃ in human preadipocyte proliferation and differentiation. Methods: RTCA, MTT, and trypan blue assays were used to assess the effects of 1,25(OH)₂D₃ on the viability, proliferation, and adipogenic differentiation of SGBS cells. Cell cycle and apoptosis analyses were performed with flow cytometry, triglycerides were quantified, and RT-qPCR was used to assess gene expression. Results: We confirmed that the SGBS cell model is suitable for studying adipogenesis and demonstrated that the differentiation protocol induces cell maturation, thereby increasing the lipid content of cells independently of treatment. 1,25(OH)₂D₃ treatment had different effects according to the cell stage, indicating different modes of action driving proliferation and differentiation. In preadipocytes, 1,25(OH)₂D₃ induced G1 growth arrest at both tested concentrations without altering CDKN1A gene expression. Treatment with 100 nM 1,25(OH)₂D₃ also decreased MTT absorbance and the lipid concentration. Moreover, increased normalized cell index values and decreased metabolic activity were not induced by proliferation or apoptosis. Exposure to 100 nM 1,25(OH)₂D₃ induced VDR, CEBPA, and CEBPB expression, even in the preadipocyte stage. During adipogenesis, 1,25(OH)₂D₃ had limited effects on processes such as VDR and PPARG gene expression, but it upregulated CEBPA expression. Conclusions: We demonstrated for the first time that 1,25(OH)₂D₃ induces changes in preadipocytes, including VDR expression and growth arrest, and increases the lipid content in adipocytes treated for 16 days. Preadipocytes are important cells in adipose tissue homeostasis, and understanding the role of 1,25(OH)₂D₃ in adipogenesis is a crucial step in ensuring adequate vitamin D supplementation, especially for obese individuals.

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Section: Discussionmentioning

confidence: 98%

Role of 1α,25-Dihydroxyvitamin D3 in Adipogenesis of SGBS Cells: New Insights into Human Preadipocyte Proliferation

Felicidade¹,

Sartori

Coort

et al. 2018

Cell Physiol Biochem

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“…effects in inhibition of inflammatory markers' gene expression (17,29). Another proposed mechanism involves the roles of these vitamins in decreasing systemic inflammation, and subsequently the GC incidence, by reducing insulin resistance (40)(41)(42)(43). In case of Vitamin B6, as this vitamin has a crucial role in amino acid and amines metabolism, it is logical to assume an essential part for this vitamin in reducing the chronic inflammation.…”

Section: Discussionmentioning

confidence: 99%

The Association Between Index of Nutritional Quality (INQ) and Gastric Cancer and Evaluation of Nutrient Intakes of Gastric Cancer Patients: A Case-Control Study

et al. 2018

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Background: Gastric cancer (GC) is the fourth major malignancy and the second leading cause of cancer-related deaths worldwide. Northern and northwestern areas of Iran are among the high risk areas for GC. Studies have shown that dietary components are implicated in the etiology of GC. The index of nutritional quality (INQ) is a method of quantitative and qualitative analysis of single foods, meals, and diets. We aimed to assess the association of INQ with GC, and to evaluate the nutrient intake of GC patients. Methods: The present case-control study included 82 cases and 95 healthy controls attending specialized centers in Tabriz, Iran, from December 2014 to May 2016. INQ scores were computed based on dietary intake assessed using a validated 168-item food frequency questionnaire (FFQ). Logistic regression models were used to estimate multivariable ORs adjusted age, gender, BMI, smoking, residency, education, and regular physical activity. Results: After controlling for several covariates, inverse associations were observed between GC risk and INQs of vitamins A, B6, and D (ORvitA = 0.25 (0.06 -0.98); ORvitB6 = 0.10 (0.04 -0.28); and ORvitD = 0.14 (0.02 -0.84)). Cases had higher intake of total fat, saturated fatty acids, beef, lamb meat, salt, and paprika compared to controls. On the other hand, controls had higher intake of vitamin A, vitamin, vitamin B6, copper, poultry, low fat milk, tea, coffee, turmeric, and saffron compared to cases. Conclusions: Subjects who follow a more healthy and nutrient-rich diet, especially in terms of vitamins A, B6, and D, are at lower risk of having GC, compared to those who consume a more unhealthy, nutrient-poor diet.

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“…Vitamin D 3 may act as an antagonist of hedgehog signaling to suppress viability of gastric cancer cells, and it also has a synergistic effect with other anticancer drugs by reducing mRNA expression of the target genes of hedgehog signaling ( Ptch1, Gli1, cyclin D1 and bcl2) [95]. Co-treatment with cisplatin and 1α,25(OH) 2 D 3 enhanced cisplatin-mediated cell growth inhibition and cell apoptosis of human gastric cancer cells with an upregulation of Bax, a decrease in ERK and AKT phosphorylation levels, and an increase in p21 and p27 levels [96]. …”

Section: Vitamin D/vdr and Gastric Cancer: Laboratorial Researchmentioning

confidence: 99%

Pathogenic roles of alterations in vitamin D and vitamin D receptor in gastric tumorigenesis

Yang

Zhao

et al. 2017

Oncotarget

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Gastric cancer is currently the second leading cause of cancer-related death worldwide, especially in Japan, Korea and China, and the 5-year survival rate of gastric cancer is less than 30%. Thus, it is important to shed more lights on novel agents to prevent gastric cancer or to improve survival rate of the patients. Vitamin D not only maintains calcium and bone homeostasis, but also mostly inhibits tumor genesis, invasion, and metastasis through activation of vitamin D receptor. Although epidemiological results are not consistent, accumulating evidence from gastric cancer cells, animal models, and clinical trials suggest that vitamin D deficiency may increase the risk and mortality of gastric cancer, but vitamin D supplement might be a safe and economical way to prevent or treat gastric cancer. Here, we reviewed the current studies on vitamin D and its receptor and focused on the pathogenic roles of their alterations in gastric tumorigenesis.

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1,25-Dihydroxyvitamin D3 and cisplatin synergistically induce apoptosis and cell cycle arrest in gastric cancer cells

Cited by 37 publications

References 40 publications

Role of 1α,25-Dihydroxyvitamin D3 in Adipogenesis of SGBS Cells: New Insights into Human Preadipocyte Proliferation

Role of 1α,25-Dihydroxyvitamin D3 in Adipogenesis of SGBS Cells: New Insights into Human Preadipocyte Proliferation

The Association Between Index of Nutritional Quality (INQ) and Gastric Cancer and Evaluation of Nutrient Intakes of Gastric Cancer Patients: A Case-Control Study

Pathogenic roles of alterations in vitamin D and vitamin D receptor in gastric tumorigenesis

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