• Asian Pacific Journal of Cancer Prevention
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• v.15 no.15
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• pp.6269-6273
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• 2014

Growing evidence suggests that miR-150-5p has an important role in regulating genesis of various types of cancer. However, the roles and the underlying mechanisms of miR-150-5p in development of colorectal cancer (CRC) remain largely unknown. Transwell chambers were used to analyze effects on cell migration and invasion by miR-150-5p. Quantitative real-time PCR (qRT-PCR), Western blotting and dual-luciferase 3' UTR reporter assay were carried out to identify the target genes of miR-150-5p. In our research, miR-150-5p suppressed CRC cell migration and invasion, and MUC4 was identified as a direct target gene. Its effects were partly blocked by re-expression of MUC4. In conclusiomn, miR-150-5p may suppress CRC metastasis through directly targeting MUC4, highlighting its potential as a novel agent for the treatment of CRC metastasis.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.8
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• pp.4675-4678
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• 2013

The aim of this study was to detect the expression of miR196a, miR146a, miR27a and miR200a in patients with colon cancer, and investigate the effect of miR27a expression on proliferation and invasion in colonic cancer cells. RT-PCR was employed to detect the expression levels in colon cancers. Then, colon cancer cells were cultured and transfected with 100 nM of miR27a mimics (80 nmol/L) or 80 nM miR27a inhibitors (80 nmol/L) in 24-well plates. Proliferation and invasion of colonic cancer cells were then determined by CCK-8 and Transwell assays, respectively. Our data showed miR27a to be high-expressed in patients with colon cancer. In addition, proliferation and invasion in the miR27a mimic group were significantly higher than in the control group and negative group (P<0.05), while, proliferation and invasion in the miR27a inhibitor group were obviously lowered (P<0.05). In conclusion, high expression of miR27a may play an important role in enhancing proliferation and invasion of colon cancer cells.

• THE JOURNAL OF KOREAN ORIENTAL ONCOLOGY
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• v.7 no.1
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• pp.109-116
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• 2001

By applying in vitro invasion assay model, we examined the anti-metatstastic effect of ChunghjagamTang(CLJGT). In 3H-thymidine incorporation assay, CLJGT treated groups showed the decreased DNA synthesis rate compared with control group. Gelatin zymogram assay showed that CLJGT decreases the gelatinolytic activity of MMP-9 from A-549, at the concentration of $800{\mu}g/ml$. We examined whether CLJGT inhibits the invasion of A-549 cells through the matrigel precoated transwell chamber. The results showed that CLJGT effectively inhibited the invasion of A-549 as compared with the control (+PMA) groups. From our research, part of mechanism underlying anti-metastastic effect of CLJGT was proven in vitro.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.9
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• pp.5391-5396
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• 2013

Aim: To investigate the role of Golgi phosphoprotein 3 (GOLPH3) in tumour growth and metastasis of esophageal squamous cancer. Methods: A lentiviral shRNA-vector was utilized to stably knockdown GOLPH3 in Eca-109 esophageal squamous cancer cells. mRNA transcription and protein expression of GOLPH3 were examined by real-time quantitative PCR and Western blotting, respectively. Cell proliferation activity was assessed by MTT assay and invasion and migration potentials by matrigel invasion and transwell motility assays. Results: Stable knockdown in the GOLPH3 cell line was established. PD-A gene expression was significantly suppressed by lentivirus-mediated RNAi, which resulted in reducing the capacity for cell proliferation, migration, invasion and adhesion in vitro. In vivo, GOLPH3 depletion resulted in inhibition of tumour growth, with stable decrease in the expression of GOLPH3 in tumor xenografts. Conclusions: Our findings suggest that lentivirus mediated silencing of the GOLPH3 gene has a significant anti-tumour effect on esophageal squamous cancer in vitro and in vivo. In addition, the results indicate that GOLPH3 might be an effective molecular target for gene therapy in esophageal squamous cancer.

• BMB Reports
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• v.49 no.9
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• pp.502-507
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• 2016

To examine the effect of TBMS1on breast cancer metastasis, and investigate the potential mechanism by which Tubeimoside-1 (TBMS1) inhibits the CXCR4 expression in breast cancer cells. The expression of CXCR4 in breast cancer cell lines was determined by immunoblotting and real-time PCR. The effect of TBMS1 on NF-κB binding activity was evaluated by EMSA assay and ChIP analysis. Cell proliferation and invasion were analyzed by MTT assay and transwell invasion assay, respectively. The effect of TBMS1 on breast cancer metastasis was further evaluated in a metastasis model of nude mice. TBMS1 suppressed the expression of CXCR4 through inhibition of NF-κB binding activity. TBMS1 inhibited CXCL12-induced invasion in breast cancer cells, while ectopic expression of CXCR4 abolished the inhibitive activity of TBMS1. TBMS1 suppressed breast cancer metastasis in the metastatic model of nude mice. TBMS1 suppressed the CXCR4-mediated metastasis of breast cancer by inhibiting NF-κB binding activity.

• Archives of Pharmacal Research
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• v.27 no.2
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• pp.127-135
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• 2004

Multiple drug administration is common in elderly, HIV, and cancer patients. Such treatments may result in drug-drug interactions due to interference at the metabolic enzyme level, and due to modulation of transporter protein functions. Both kinds of interference may result in altered drug distribution and toxicity in the human body. In this review, we have dealt with drug-drug interactions related to the most studied human transporter, P-glycoprotein. This transporter is constitutively expressed in several sites in the human body. Its function can be studied in vitro with different cell lines expressing P-glycoprotein in experiments using methods and equipment such as flow cytometry, cell proliferation, cell-free ATP as activity determination and Transwell culture equipment. In vivo experiments can be carried out by mdr1a(-/-) animals and by noninvasive methods such as NMR spectrometry. Some examples are also given for determination of possible drug-drug interactions using the above-mentioned cell lines and methods. Such preclinical studies may influence decisions concerning the fate of new drug candidates and their possible dosages. Some examples of toxicities obtained in clinics and summarized in this review indicate careful consideration in cases of polypharmacy and the requirement of preclinical studies in drug development activities.

• BMB Reports
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• v.52 no.5
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• pp.312-317
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• 2019

Hepatocellular carcinoma (HCC) is the leading cause of cancer-related mortality worldwide. MiR-371 has recently emerged as an important regulator in tumorigenesis, and may serve as a biomarker for malignant tumors. We transfected miR-371 or its inhibitor in two human HCC cell lines, then used 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, soft agar colony formation, and transwell migration assays to evaluate the effects on cell proliferation, migration, and invasion. We found that miR-371 was positively correlated with HCC metastasis and poor prognosis in the inflicted patients, and the high expression of miR-371 was promoted, whereas a low level of miR-371 depressed cell proliferation and invasion. We found PTEN to be a direct target of miR-371. The overexpression or knockdown of PTEN exhibited the opposite effects from those of miR-371 on cell proliferation and migration. Our study demonstrates that miR-371 promotes proliferation and metastasis in HCC by targeting PTEN.

• Journal of Microbiology and Biotechnology
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• v.31 no.6
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• pp.784-793
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• 2021

Previous studies have uncovered the role of circ_0000144 in various tumors. Here, we investigated the function and mechanism of circ_0000144 in gastric cancer (GC) progression. The expression of circ_0000144 in GC tissues and cells was detected through quantitative real-time polymerase chain reaction (qRT-PCR) method. Gain- and loss-of-function experiments including colony formation, wound healing and transwell assays were performed to examine the role of circ_0000144 in GC cells. Furthermore, western blot was conducted to determine the expressions of epithelial mesenchymal transition (EMT)-related proteins. The interaction between circ_0000144 and miR-217 was analyzed by bioinformatic analysis and luciferase reporter assays. The circ_0000144 expression was obviously upregulated in GC tissues and cells. Silencing of circ_0000144 inhibited cell proliferation, migration and invasion of GC cells, but ectopic expression of circ_0000144 showed the opposite results. Moreover, circ_0000144 sponged miR-217, and rescue assays revealed that silencing miR-217 expression reversed the inhibitory effect of circ_0000144 knockdown on the progress of GC. Our findings reveal that circ_0000144 inhibition suppresses GC cell proliferation, migration and invasion via absorbing miR-217, providing a new biomarker and potential therapeutic target for treatment of GC.

• Journal of Physiology & Pathology in Korean Medicine
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• v.35 no.5
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• pp.177-184
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• 2021

The root bark of Morus alba L. (MA) used in traditional oriental medicine for the treatment of pulmonary diseases exerts various pharmacological activities including anticancer effects. In the current study, we investigated the effects of MA on the migration and invasion of colorectal carcinoma cells. Results from a transwell assay showed that the methylene chloride extract of MA (MEMA) suppressed the migration and invasion of HCT116 human colorectal carcinoma cells in a concentration-dependent manner. MEMA reduced both mRNA and protein levels of matrix metalloproteinase (MMP)-9, but did not suppress the expression of MMP-2 in HCT116 cells. As a molecular mechanism, MEMA inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs), including ERK, JNK and p38, in a dose-dependent manner. In addition, MEMA dephosphorylated both Src and signal transducer and activator of transcription 3 (STAT3) in HCT116 cells. Taken together, we demonstrate that MEMA suppressed the migration and invasion capacity of HCT116 human colorectal cancer cells by downregulation of MMP-9 and inactivation of both MAPKs and Src/STAT3 signaling pathway.

• The Korean Journal of Physiology and Pharmacology
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• v.28 no.4
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• pp.379-387
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• 2024

Breast cancer (BC) is most commonly diagnosed worldwide. Liquiritigenin is a flavonoid found in various species of the Glycyrrhiza genus, showing anti-tumor activity. This article was to explore the influences of liquiritigenin on the biological behaviors of BC cells and its underlying mechanism. BC cells were treated with liquiritigenin alone or transfected with oe-HSP90 before liquiritigenin treatment. RT-qPCR and Western blotting were employed to examine the levels of HSP90, Snail, E-cadherin, HSC70, and LAMP-2A. Cell viability, proliferation, migration, and invasion were evaluated by performing MTT, colony formation, scratch, and Transwell assays, respectively. Liquiritigenin treatment reduced HSP90 and Snail levels and enhanced E-cadherin expression as well as inhibiting the proliferation, migration, and invasion of BC cells. Moreover, liquiritigenin treatment decreased the expression of HSC70 and LAMP-2A, proteins related to chaperone-mediated autophagy (CMA). HSP90 overexpression promoted the CMA, invasion, and migration of BC cells under liquiritigenin treatment. Liquiritigenin inhibits HSP90-mediated CMA, thereby suppressing BC cell growth.