• 동의생리병리학회지
• /
• 제25권3호
• /
• pp.466-470
• /
• 2011

The purpose of this study was to investigate the anti-cancer effects of Carthami Flos in some kinds of human gastric cancer cells. We used two kinds of human gastric cancer cell lines, such as AGS cells and MKN45 cells. We examined cell death by MTT assay and observed the morphological changes with Carthami Flos. Also, we showed that the combination of sub-optimal doses of Carthami Flos and cisplatin noticeably suppresses in AGS cells and doxorubicin in MKN45 cells. Furthermore, we studied the caspase 3 activity to identify the apoptosis. Therefore, our findings provide insight into unraveling the effects of Carthami Flos in human gastric cancer cells and developing therapeutic agents against gastric cancer.

• 대한예방한의학회지
• /
• 제15권3호
• /
• pp.127-140
• /
• 2011

Objectives : The research was conducted to confirm the effect of Acanthopanax senticosus harms(ASH) on the anti-tumor activities in AGS human gastric cancer cells. Methods : To examine the potential anti-tumor effect of ASH, we performed many experiments. After processing AGS cancer cells with varying concentrations 80% ethanol ASH extract, analyses by MTT, flow cytometer(FACS) and western blot were used. Results : AGS cancer cells showed decreased cell proliferation and increased contents of S phase when treated with ASH. Moreover, the Western blot experiment showed that ASH affected S phase cell cycle-related molecules(Cyclin A, p21 and p16) in AGS cells. ASH also inhibited EGFR-STAT3 pathway in AGS human gastric cancer cells. Conclusion : Based on these results, we observed that ASH arrested the cell cycle at S phase and inhibited the phosphorylation of EGFR and STAT3 proteins which reduce the cell cycle and the manifestation of the genes that are related to inhibiting cell growth in AGS cells. It can be concluded that ASH can be used in developing medicine for gastric cancer.

• Journal of Gastric Cancer
• /
• 제20권3호
• /
• pp.300-312
• /
• 2020

Purpose: Circular RNAs (circRNAs) are a new class of RNA molecules whose function is largely unknown. There is a growing evidence that circRNAs play an important regulatory role in the progression of a variety of human cancers. However, the exact roles and the mechanisms of circRNAs in gastric cancer are not clear. In this study, we aimed to elucidate the mechanism of hsa_circ_0005556. Materials and Methods: Real-time quantitative polymerase chain reaction was used to detect the expression of hsa_circ_0005556, miR-4270, and matrix metalloproteinase-19 (MMP19) in gastric cancer tissues and cell lines. The expression of hsa_circ_0005556 in gastric cancer cells was silenced by lentivirus, and cell proliferation, invasion, migration, and tumorigenesis in nude mice were assessed to evaluate the function of hsa_circ_0005556 in gastric cancer. Results: The expression of hsa_circ_0005556 in gastric cancer tissues and gastric cancer cell lines was higher compared to normal controls. In vitro, the downregulation of hsa_ circ_0005556 significantly inhibited proliferation, migration, and invasion of gastric cancer cells. In vivo, the downregulation of hsa_circ_0005556 suppressed tumor growth in nude mice. Conclusions: Our study shows that the hsa_circ_0005556/miR-4270/MMP19 axis is involved in proliferation, migration, and invasion of gastric cancer cells through the competing endogenous RNA (ceRNA) mechanism.

• Journal of Gastric Cancer
• /
• 제13권3호
• /
• pp.172-178
• /
• 2013

Purpose: The aims of this study were as follow: 1) to de scribe the expression status of estrogen receptor-${\alpha}$ and -${\beta}$ mRNAs in five gastric carcinoma cell lines; 2) to evaluate in vitro the effects of $17{\beta}$-estradiol and estrogen receptor antagonists on the proliferation of the cell lines. Materials and Methods: Detection of estrogen receptor-${\alpha}$ and estrogen receptor-${\beta}$ mRNA in five human gastric cancer cell lines (AGS, KATO III, MKN28, MKN45 and MKN74) was made by the reverse transcription-polymerase chain reaction system. To evaluate the effect of $17{\beta}$-estradiol and estrogen receptor antagonists on the proliferation of gastric cancer cell line, the cell lines which expressed both es trogen receptors were chosen and treated with $17{\beta}$-estradiol and estrogen receptor antagonists (methyl-piperidino-pyrazole and pyrazolo [1,5-a] pyrimidine). Cell proliferation was assessed with the methylthiazol tetrazolium test. Results: Estrogen receptor-${\alpha}$ and estrogen receptor-${\beta}$ mRNAs were expressed in three (KATO III, MKN28 and MKN45) and all of the five gastric cancer cell lines, respectively. At higher concentrations, $17{\beta}$-estradiol inhibited cell growth of MKN28, MKN45 and KATO III cell lines. Neither estrogen receptor-${\alpha}$ nor estrogen receptor-${\beta}$ antagonist blocked the anti-proliferative effect of $17{\beta}$-estradiol. Conclusions: Our results indicate that estrogen receptor-${\beta}$ mRNAs are preferentially expressed in gastric cancers and also imply that hormone therapy rather than estrogen receptor blockers may be a useful strategy for the treatment of estrogen receptor-${\beta}$ positive gastric cancer. Its therapeutic significance in gastric cancer are, however, limited until more evidence of the roles of estrogen receptors in the gastric cancer are accumulated.

• Asian Pacific Journal of Cancer Prevention
• /
• 제13권4호
• /
• pp.1377-1382
• /
• 2012

Morphine is not only an analgesic treating pain for patients with cancer but also a potential anticancer drug inhibiting tumor growth and proliferation. To gain better insight into the involvement of morphine in the biological characteristics of gastric cancer, we investigated effects on progression of gastric carcinoma cells and the expression of some apoptosis-related genes including caspase-9, caspase-3, survivin and NF-${\kappa}B$ using the MGC-803 human gastric cancer cell line. The viability of cells was assessed by MTT assay, proliferation by colony formation assay, cell cycle progression and apoptosis by flow cytometry and ultrastructural alteration by transmission electron microscopy. The influences of morphine on caspase-9, caspase-3, survivin and NF-${\kappa}B$ were evaluated by semi-quantitative RT-PCR and Western blot. Our data showed that morphine could significantly inhibit cell growth and proliferation and cause cell cycle arrest in the G2/M phase. MGC-803 cells which were incubated with morphine also had a higher apoptotic rate than control cells. Morphine also led to morphological changes of gastric cancer cells. The mechanism of morphine inhibiting gastric cancer progression in vitro might be associated with activation of caspase-9 and caspase-3 and inhibition of survivin and NF-${\kappa}B$.

• Journal of Gastric Cancer
• /
• 제7권2호
• /
• pp.59-66
• /
• 2007

목적: 위암 세포주 및 조직에서 다중 표지자 mRNA 발현을 정량적 RT-PCR 검사를 통해 확인함으로써 이들 표지자를 이용하여 위암의 복강내 미세전이 진단이 가능한가를 평가하고자 본 연구를 시행하였다. 대상 및 방법: 12개의 인체 위암 세포주와 10개의 위암 조직을 대상으로 Carcinoembryonic antigen (CEA), Cytokeratin 20 (CK20), Dopa decarboxylase (DDC), L-3-phosphoserine phosphatase (L3PP)의 네 가지 mRNA를 이용한 정량적 RT-PCR 다중 표지자 분석을 시행하였다. 결과: 12개의 인체 위암 세포주 중 CEA는 4개(33%), CK-20는 1개(8%), DDC는 6개(50%), L3PP는 12개 세포주 모두(100%)에서 과발현되었다. 10개의 위암 조직 중 CEA는 9개, CK20은 3개, DDC는 9개, L3PP는 10개 조직 모두에서 과발현되었다. L3PP는 모든 위암 세포주와 조직에서 과발현을 나타내었으나 과발현 정도는 비교적 낮게 측정된 반면, CEA와 DDC는 일부 위암 세포주 및 조직에서만 과발현을 나타내었지만 파발현 시 충분한 발현도를 나타내었다. 결론: 위암 환자에서 하나 이상의 암 특이적 유전자를 이용한 다중 표지자 분석은 단일 표지자 분석이 가지는 단점을 보완할 수 있을 것으로 예상되며, CEA, DDC, 및 L3PP의 세 가지 mRNA가 후보 유전자로 사용될 수 있을 것으로 생각한다.

• Asian Pacific Journal of Cancer Prevention
• /
• 제13권4호
• /
• pp.1425-1430
• /
• 2012

Cyclin L2 is a novel member of the cyclin family, recently implicated in the regulation of cell cycle progression and/or transcriptional regulation. The present study was undertaken to investigate the effects of overexpression on tumor cell growth and chemosensitivity in human gastric cells in vitro. Cyclin L2 was transfected into human gastric cancer cell line BCG823 and expressed with a mammalian expression vector pcDNA3.1. The effects and mechanisms of cyclin L2 on cell growth, cell cycling and apoptosis were studied. Compared to control vectors, overexpression of cyclin L2 inhibited the growth of BCG823 cells and enhance their chemosensitivity to fluorouracil, docetaxel and cisplatin. The anti-proliferative effects of cyclin L2 could be due to G0/G1 arrest and apoptosis. Cyclin L2 induced G0/G1 arrest and apoptosis involved upregulation of caspase-3 and down regulation Bcl-2 and survivin. The results indicated that overexpression of cyclin L2 protein may promote efficient growth inhibition and enhance chemosensitivity to chemotherapeutic agents in human gastric cancer cells by inducing G0/G1 cell cycle arrest and apoptosis.

• 생명과학회지
• /
• 제31권12호
• /
• pp.1057-1065
• /
• 2021

위암 환자에서 미토콘드리아 DNA (mtDNA)의 양적 변화가 보고 되고 있으며 이러한 변화가 위암의 발암이나 진행에 관여되는 것으로 추정되고 있다. 그리나 위암에서 미토콘드리아 단백질이나 mtDNA에 의해 암호화된 산화적 인산화(OXPHOS) 단백질의 양적 변화에 관한 연구는 아직까지 미비한 실정이다. 본 연구에서는 위암환자 조직 및 세포주를 이용하여 mtDNA 양 그리고 미토콘드리아 단백질 및 OXPHOS 단백질의 양을 분석하였다. 또한, mtDNA 양적 변화와 위암 환자의 임상병리학적 특징을 연관 분석하였다. MtDNA 양을 분석하기 위하여 qPCR 기법을 그리고 단백질 분석에는 Western blot 기법을 각각 활용하였다. 총 27개의 위암 환자 샘플에서 약 80%에 해당하는 22개의 환자 위암조직에서 정상조직에 비해 mtDNA 양이 감소하였으며, 나머지 환자에서는 mtDNA 양이 증가하였다. 이러한 mtDNA 양이 감소한 위암 조직 샘플에서는 미토콘드리아 단백질 및 OXPHOS 단백질의 양도 같이 감소하였다. 한편, 본 연구에 사용된 총 5개의 위암 세포주 모두에서 mtDNA 양이 감소하였다 그러나 위암 세포주에서는 mtDNA 양적 감소와 미토콘드리아 단백질 및 OXPHOS 단백질의 양적 감소가 항상 일치하지는 않았다. 이러한 연구결과는 위암 조직 및 세포주에서 mtDNA 양의 감소가 흔하며 이는 mtDNA 양적 변화가 위암의 생성에 관여함을 제시한다.

• BMB Reports
• /
• 제47권12호
• /
• pp.697-702
• /
• 2014

Recently, the interest in natural products for the treatment of cancer is increasing because they are the pre-screened candidates. In the present study, we demonstrate the therapeutic effect of celastrol, a triterpene extracted from the root bark of Chinese medicine on gastric cancer. The proliferation of AGS and YCC-2 cells were most sensitively decreased in six kinds of gastric cancer cell lines after the treatment with celastrol. Celastrol inhibited the cell migration and increased G1 arrest in cell-cycle populations in both cell lines. The treatment with celastrol significantly induced autophagy and apoptosis and increased the expression of autophagy and apoptosis-related proteins. We also found an increase in phosphorylated AMPK following a decrease in all phosphorylated forms of AKT, mTOR and S6K after the treatment with celastrol. Moreover, gastric tumor burdens were reduced in a dose-dependent manner by celastrol administration in a xenografted mice model. Taken together, celastrol distinctly inhibits the gastric cancer cell proliferation and induces autophagy and apoptosis.

• Journal of Gastric Cancer
• /
• 제14권3호
• /
• pp.147-155
• /
• 2014

Homeostatic imbalance between cell proliferation and death in gastric mucosal epithelia may lead to gastritis and gastric cancer. Despite abundant gastrokine 1 (GKN1) expression in the normal stomach, the loss of GKN1 expression is frequently detected in gastric mucosa infected with Helicobacter pylori, as well as in intestinal metaplasia and gastric cancer tissues, suggesting that GKN1 plays an important role in gastric mucosal defense, and the gene functions as a gastric tumor suppressor. In the stomach, GKN1 is involved in gastric mucosal inflammation by regulating cytokine production, the nuclear factor-${\kappa}B$ signaling pathway, and cyclooxygenase-2 expression. GKN1 also inhibits the carcinogenic potential of H. pylori protein CagA by binding to it, and up-regulates antioxidant enzymes. In addition, GKN1 reduces cell viability, proliferation, and colony formation by inhibiting cell cycle progression and epigenetic modification by down-regulating the expression levels of DNMT1 and EZH2, and DNMT1 activity, and inducing apoptosis through the death receptor-dependent pathway. Furthermore, GKN1 also inhibits gastric cancer cell invasion and metastasis via coordinated regulation of epithelial mesenchymal transition-related protein expression, reactive oxygen species production, and PI3K/Akt signaling pathway activation. Although the modes of action of GKN1 have not been clearly described, recent limited evidence suggests that GKN1 acts as a gastricspecific tumor suppressor. This review aims to discuss, comment, and summarize the recent progress in the understanding of the role of GKN1 in gastric cancer development and progression.