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Revista de la Facultad de Medicina Humana

versión impresa ISSN 1814-5469versión On-line ISSN 2308-0531

Rev. Fac. Med. Hum. vol.23 no.3 Lima jul./set. 2023  Epub 21-Sep-2023

http://dx.doi.org/10.25176/rfmh.v23i3.5904 

Letter to the Editor

Can vitamin d be the ray of sunshine that lights up the treatment of gastric cancer?

Alfredo W. Campos Perez1 

Sacha Barrios Healey2 

José M. Vela Ruiz1  3 

1Instituto de Investigaciones en ciencias biomédicas, Universidad Ricardo Palma. Lima- Perú

2Universidad de Medicina Tradicional China. Nanjing, China.

2Unidad de oncología y prevención, Hospital San Juan de Lurigancho, Lima-Perú

Mr. Editor:

Gastric cancer, a malignant neoplasm that originates in the cells of the stomach lining, represents a significant burden in terms of mortality worldwide. According to data from the American Cancer Society, the estimated mortality rate is 4.9 per 100,000 people in 2021. In South America, mortality rates from gastric cancer continue to be of concern, with countries such as Chile and Peru reporting mortality rates of 18.7 and 13.6 per 100,000 persons respectively in 20211.

Gastric cancer being a major pathology mentioned in other previously published studies2.

Vitamin D is a fat-soluble hormone that occurs in two main forms, D2 (ergocalciferol) and D3 (cholecalciferol). It is produced in the skin under exposure to ultraviolet light or derived from plant sterol. It is metabolized in the liver and kidney to active forms. In addition to its role in calcium homeostasis, studies suggest that vitamin D has anticancer effects by inhibiting cell proliferation and promoting apoptosis. Thus, there is increasing interest as a potential anticancer agent3.

Studies have demonstrated the therapeutic potential of vitamin D3 in gastric cancer. An in vitro and in vivo study found that vitamin D3 suppresses the growth of gastric cancer cells by down-regulating the expression of CD444. In addition, another study showed that vitamin D3 affects gastric cancer progression by repressing BMP3 promoter methylation5.

Raising vitamin D levels to 42 ng/mL is estimated to reduce disease rates and mortality in various cancers by 18% per year6. Inactivation of Wnt/beta-catenin signaling, induction of cell apoptosis, and inhibition of cell invasion and cancer metastasis are some of the mechanisms described6. Some studies are described in Table 1.

Although the antitumor effects of vitamin D3 have been demonstrated in preclinical studies, there is still a lack of adequately designed clinical studies evaluating the safety and efficacy of vitamin D3 in gastric cancer. In addition, further studies on the antitumor effects of vitamin D3 in gastric cancer are needed to develop more effective therapeutic strategies4-6.

Table 1 A table describing studies exploring the involvement of vitamin D in gastric cancer. 

Author Country Type of study Population MEChANIS Benefits
Li et al.4 China In vivo Nude (nu/nu) mice with xenogeneic GC tumors. Oral administration of VD like intraperitoneal injection of 1,25(OH)2D3 significantly inhibited orthotopic gastric cancer growth and CD44 expression in vivo. VD significantly inhibited tumor growth in treated mice compared to untreated controls.
Li et al.4 China In vitro Human GC cell lines MKN45 and AGS VD 1,25(OH)2D3 suppressed MKN45 and KATO III cell growth through VDR-induced suppression of CD44. Significantly decreased cell growth and CD44 expression in VD-treated cells.
Zhao et al.5 China In vitro BGC-823, SGC-7901, MGC80-3, AGS-1 and MKN-28 cell lines. Cell proliferation was measured by cell viability assays and cell migration and invasion were assessed by scratch and transwell assays. In addition, cell cycle and apoptosis were analyzed by flow cytometry. VD increases BMP3 expression and delays GC progression.
Chang et al.7 China In vitro SGC-7901 human GC cell line and cultured with RPIM1640 containing 10% fetal bovine serum (FBS). Activation of the VDR receptor by 1,25(OH)2D3 to induce miR-99b-VDRE expression in GC cells in vitro. VD inhibits GC cell proliferation by increasing miR-99b-3p expression.

VD: vitamin D; GC: gastric cancer; BMP3: bone morphogenetic protein; VDBP: vitamin D-binding protein; VDR: vitamin D receptor; VDD: vitamin D deficiency; VDBP: vitamin D-binding protein; VDR: vitamin D receptor; VDDD: vitamin D deficiency; VDBP: vitamin D-binding protein.

REFERENCES

1. American Cancer Society | Cancer Facts & Statistics [Internet]. American Cancer Society | Cancer Facts & Statistics. [citado el 9 de abril de 2023]. Disponible en: http://cancerstatisticscenter.cancer.org/ [ Links ]

2. Ramos AR, Sánchez RS. Helicobacter pylori y cáncer gástrico. Revista de Gastroenterología del Perú. 2008;258-66. doi: 10.47892/rgp.2008.283.516 [ Links ]

3. Nguyen MT, Huynh NNY, Nguyen DD, Ta NH, Van Nguyen T, Dang HT, et al. Vitamin D intake and gastric cancer in Viet Nam: a case-control study. BMC Cancer. 2022;22(1):838. doi: 10.1186/s12885-022-09933-2 [ Links ]

4. Li Q, Li Y, Jiang H, Xiao Z, Wu X, Zhang H, et al. Vitamin D suppressed gastric cancer cell growth through downregulating CD44 expression in vitro and in vivo. Nutrition. 2021;91-92:111413. doi: 10.1016/j.nut.2021.111413 [ Links ]

5. Zhao Y, Cai L-L, Wang H-L, Shi X-J, Ye H-M, Song P, et al. 1,25-Dihydroxyvitamin D3 affects gastric cancer progression by repressing BMP3 promoter methylation. Onco Targets Ther. 2019;12:2343-53. doi: 10.2147/OTT.S195642 [ Links ]

6. Bashir M, Prietl B, Tauschmann M, Mautner SI, Kump PK, Treiber G, et al. Effects of high doses of vitamin D3 on mucosa-associated gut microbiome vary between regions of the human gastrointestinal tract. Eur J Nutr. 2016;55(4):1479-89. doi: 10.1007/s00394-015-0966-2 [ Links ]

7. Chang S, Gao Z, Yang Y, He K, Wang X, Wang L, et al. miR-99b-3p is induced by vitamin D3 and contributes to its antiproliferative effects in gastric cancer cells by targeting HoxD3. Biological Chemistry. 2019;400(8):1079-86. doi: 10.1515/hsz-2019-0102 [ Links ]

Funding: Self-financed.

8Article published by the Journal of the faculty of Human Medicine of the Ricardo Palma University. It is an open access article, distributed under the terms of the Creatvie Commons license: Creative Commons Attribution 4.0 International, CC BY 4.0 (https://creativecommons.org/licenses/by/1.0/), that allows non-commercial use, distribution and reproduction in any medium, provided that the original work is duly cited. For commercial use, please contact revista.medicina@urp.edu.pe.

Received: April 02, 2023; Accepted: July 04, 2023

Correspondence author: Alfredo Williams Campos Perez Address: Avenida Benavides 5440, Santiago de Surco, Lima 33-Perú. Phone: +51 989022921 E-mail:alfredow.campos@gmail.com

Author contributions: All authors participated in the conception, preparation, and approval of the final version of the manuscript.

Declaration of conflict of interest: None.

Creative Commons License Este es un artículo publicado en acceso abierto bajo una licencia Creative Commons

 
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