Journal of Yeungnam Medical Science

Review article

The role of microRNAs in cell death pathways: Ji Hoon Jang, Tae-Jin Lee; Yeungnam Univ J Med. 2021;38(2):107-117. Published online January 13, 2021; DOI: https://doi.org/10.12701/yujm.2020.00836

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MicroRNAs (miRNAs) are a class of noncoding RNAs that negatively regulate target messenger RNAs. In multicellular eukaryotes, numerous miRNAs perform basic cellular functions, including cell proliferation, differentiation, and death. Abnormal expression of miRNAs weakens or modifies various apoptosis pathways, leading to the development of human cancer. Cell death occurs in an active manner that maintains tissue homeostasis and eliminates potentially harmful cells through regulated cell death processes, including apoptosis, autophagic cell death, and necroptosis. In this review, we discuss the involvement of miRNAs in regulating cell death pathways in cancers and the potential therapeutic functions of miRNAs in cancer treatment.

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Original Articles

Apoptosis Induced by 4-HPR on Human Stomach Adenocarcinoma Cell Line SNU1: Hyou Youn Kim, Sang Woon Kim, Seong Yong Kim; Yeungnam Univ J Med. 2007;24(2 Suppl):S606-616. Published online December 31, 2007; DOI: https://doi.org/10.12701/yujm.2007.24.2S.S606

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Abstract PDF: Purpose：Retinoids derived from vitamin A have diverse effects on development, morphogenesis, and homeostasis. They also have effects for prevention and treatment of cancers. In this study, the effect of N-(4-hydroxyphenyl) retinamide (4-HPR) on growth and/or proliferation of human gastric adenocarcinoma cell line SNU1 was investigated. Materials and Methods：The cytotoxic effect of 4-HPR was assessed by MTT assay. The apoptosis induced by 4-HPR was analyzed with cytoplasmic DNA Fragmentation, flow cytometry, and Western blot.
Results
：4-HPR induced cell death of SNU1. The cytoplasmic DNA fragmentation was increased time dependently after treatment of 4-HPR and the cells in the sub-G₀/G₁ fraction of flow cytometric analysis were also increased time dependently after treatment of 4-HPR. The cleavage of caspase 3 and PARP were detected after treatment of 4-HPR to SNU1. The phosphorylations of Raf, ERK and AKT were induced by 4-HPR but after pre-treatment of MAPK inhibitor (PD98059) or PI-3 kinase inhibitor (LY294002) the 4-HPR-induced cytoplasmic DNA fragmentation, the cells in the sub-G0/G1 fraction fraction of flow cytometric analysis, and cleavage of caspase 3 and PARP were diminished in SNU1 cells.
Conclusion
：The results show that 4-HPR induces apoptosis of SNU1 and this 4-HPRinduced apoptosis may be mediated through ERK1/2 and PI3 kinase signaling pathways in SNU1.

Anticancer Effects of Gleditsin in Human Mammary Cancer Cells: Hyun Sook Ko, Kyung Won Kang, Jung Hye Kim; Yeungnam Univ J Med. 2007;24(2 Suppl):S580-590. Published online December 31, 2007; DOI: https://doi.org/10.12701/yujm.2007.24.2S.S580

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Abstract PDF: Background
：Gleditsin is a herb medicine from extracted by Gleditschia spina. In oder to investigate anticancer effects of gleditsin in human various breast cancer cells, we tested with gleditsin on cytotoxicity of materials, observed to cell survival and cell cycle progression, and analyzed in starvation condition. Materials and Methods：The cytoxicity and cell cycle progression were analyzed in human breast cells, MCF-10A and human breast cancer cell lines, MDA-MB-231, MDA-MB-361, and MDA-MB-435. IC50s of breast cancer cell lines were measured by MTT assay. The cell cycle were showed by flow cytometric analysis in cells treated with gleditsin. We analyzed DNA content of sub-Go/G1 phase, it was detected apoptosis.
Results
：Cell survivals were decreased in a dose-dependent manner by the treatment of cells with gleditsin. IC50s were 4.11-fold higher in MDA-MB-435, 2.53-fold higher in MDAMB- 231, and 2.55-fold higher in MDA-MB-361 than in normal breast cells. Flow cytometric analysis showed that sub-G0/G1 fractions in cancer cells treated with gleditsin were higher than that normal cells, suggesting that increases in cytotoxicity of cancer cells by gleditsin were resulted from apoptosis. Cell cycle progression was also changed by the treatment of gleditsin. The treatments of gleditsin resulted in a decrease in G1 phase and an increase in G2/M phase in normal breast cells as well as cancer cell lines. Apoptotic cell death was synergistically increased by cell starvation and gleditsin treatments in cancer cells. MDAMB- 435 cells were more sensitive to apoptotic cell death by gleditsin than other cells.
Conclusion
：An anti-tumor effect of gleditsin was selectively higher in hman breast cancer cells than in normal human breast cells, and was mediated by apoptotic cell death.

Profile of Gene Expression Changes During Doxorubicin Induced Apoptosis of Saos-2.: Jeong Sook Lim, Min Jae Bae, Suk Hwan Baek, Jae Ryong Kim, Jung Hye Kim, Seong Yong Kim; Yeungnam Univ J Med. 2005;22(2):221-240. Published online December 31, 2005; DOI: https://doi.org/10.12701/yujm.2005.22.2.221

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Abstract PDF: BACKGROUND
Doxorubicin has proved to be a useful chemotherapeutic agent especially for osteogenic sarcoma. It induces cancer cell death via apoptosis. MATERIALS AND METHODS: To explore and analyze the changes of gene expression during doxorubicin induced apoptosis on human osteogenic sarcoma, Saos-2 cell, cDNA microarray was performed. After treatment with doxorubicin, total RNA was purified and expressed genes were investigated with a 17k human cDNA microarray. RESULTS: For analysis of the cDNA microarray, the genes were filtered using the sum of the median value of Cy3 and Cy5 signal intensity of greater than 800. Expression of 264 genes was changed by more than 2 fold, and the expression of 35 genes was changed more than 3 fold after treatment with doxorubicin. The genes were primarily related to cell death, cell growth and maintenance, signal transduction, cellular component, transport, and metabolism. CONCLUSION: Treatment with doxorubicin induced expressional change of many genes. Some of the genes might be related with apoptosis directly or indirectly. Further study is now needed to characterize these genes.

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