Publications by authors named "Chung-Yu Yeh"

6 Publications

  • Page 1 of 1

Metformin inhibits gastric cancer cell proliferation by regulation of a novel Loc100506691-CHAC1 axis.

Mol Ther Oncolytics 2021 Sep 19;22:180-194. Epub 2021 Aug 19.

Department of Research, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, New Taipei City 23124, Taiwan.

Long noncoding RNAs (lncRNAs) are a group of nonprotein coding transcripts that play a critical role in cancer progression. However, the role of lncRNA in metformin-induced inhibition of cell growth and its biological function in gastric cancer remain largely unknown. In this study, we identified an oncogenic lncRNA, Loc100506691, the expression of which was decreased in gastric cancer cells with metformin treatment. Moreover, Loc100506691 was significantly overexpressed in gastric cancer compared with adjacent normal tissues (p < 0.001), and high Loc100506691 expression was significantly correlated with poor survival of patients with gastric cancer. Additionally, Loc100506691 knockdown could significantly suppress gastric cancer cell growth , and ectopic Loc100506691 expression accelerated tumor growth in an mouse model. Analysis of the cell cycle revealed that Loc100506691 knockdown induced cell cycle arrest at the G2/M phase by impairing cell entry from the G2/M to G1 phase. Loc100506691 negatively regulated CHAC1 expression by modulating miR-26a-5p/miR-330-5p expression, and CHAC1 knockdown markedly attenuated Loc100506691 knockdown-induced gastric cancer cell growth and motility suppression. We concluded that anti-proliferative effects of metformin in gastric cancer may be partially caused by suppression of the Loc100506691-miR-26a-5p/miR-330-5p-CHAC1 axis.
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http://dx.doi.org/10.1016/j.omto.2021.08.006DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8416970PMC
September 2021

Using Simple-Structured Split Aptamer for Gold Nanoparticle-based Colorimetric Detection of Estradiol.

Anal Sci 2021 Mar 4;37(3):479-484. Epub 2020 Dec 4.

Department of Medical Biotechnology and Laboratory Sciences, College of Medicine, Chang Gung University.

Demand for the detection of estradiol, which is a naturally occurring hormone, has been increasing. Gold nanoparticle-based colorimetric aptasensors have been developed for estradiol detection; however, the long sequence of aptamers due to the formation of the secondary structure likely affects the sensitivity of the aptasensors. Herein, a sensitive colorimetric biosensor is developed for label-free detection of estradiol by using an estradiol-specific split aptamer. The results demonstrate that a superior response is observed when a split aptamer with a high free energy of the secondary structure (ΔG > -3 kcal/mol) is used, in comparison to that observed using a split aptamer with a low free energy of the secondary structure (ΔG < -3 kcal/mol) at 27°C. After selecting the appropriate split aptamer, the standard calibration curve obtained for estradiol has a detection limit of 6.7 nM, with a linear range of 6.7 nM - 66.7 μM in the logarithmic scale. Furthermore, this assay is sensitive, easy-to-operate, inexpensive, and non-time-consuming (provides results within 50 min), thereby showing potential for clinical applications (detection of other small molecular targets).
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http://dx.doi.org/10.2116/analsci.20SCP07DOI Listing
March 2021

Involvement of MicroRNA-1-FAM83A Axis Dysfunction in the Growth and Motility of Lung Cancer Cells.

Int J Mol Sci 2020 Nov 22;21(22). Epub 2020 Nov 22.

Division of Chest Medicine, Kaohsiung Municipal Min-Sheng Hospital, Kaohsiung 802213, Taiwan.

Lung cancer is the most prevalent types of cancer and the leading cause of cancer-related deaths worldwide. Among all cancers, lung cancer has the highest incidence, accompanied by a high mortality rate at the advanced stage. Favorable prognostic biomarkers can effectively increase the survival rate in lung cancer. Our results revealed (Family with sequence similarity 83, member A) overexpression in lung cancer tissues compared with adjacent normal tissues. Furthermore, high expression was closely associated with poor lung cancer survival. Here, through siRNA transfection, we effectively inhibited expression in the lung cancer cell lines H1355 and A549. FAM83A knockdown significantly suppressed the proliferation, migration, and invasion ability of these cells. Furthermore, knockdown could suppress Epidermal growth factor receptor (EGFR)/Mitogen-activated protein kinase (MAPK)/Choline kinase alpha (CHKA) signaling activation in A549 and H1355. By using a bioinformatics approach, we found that overexpression in lung cancer may result from miR-1-3p downregulation. In summary, we identified a novel axis could partially modulate the EGFR/choline phospholipid metabolism signaling pathway, which suppressed lung cancer growth and motility. Our findings provide new insights for the development of lung cancer therapeutics.
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http://dx.doi.org/10.3390/ijms21228833DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7700477PMC
November 2020

The Long Noncoding RNA LOC441461 (STX17-AS1) Modulates Colorectal Cancer Cell Growth and Motility.

Cancers (Basel) 2020 Oct 28;12(11). Epub 2020 Oct 28.

Department of Research, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, New Taipei City 23124, Taiwan.

Colorectal carcinoma (CRC) is one of the most prevalent cancers worldwide and has a high mortality rate. Long noncoding RNAs (lncRNAs) have been noted to play critical roles in cell growth; cell apoptosis; and metastasis in CRC. This study determined that LOC441461 expression was significantly higher in CRC tissues than in adjacent normal mucosa. Pathway enrichment analysis of LOC441461-coexpressed genes revealed that LOC441461 was involved in biological functions related to cancer cell growth and motility. Knockdown of the LOC441461 expression significantly suppressed colon cancer cell growth by impairing cell cycle progression and inducing cell apoptosis. Furthermore, significantly higher LOC441461 expression was discovered in primary colon tumors and metastatic liver tumors than in the corresponding normal mucosa, and LOC441461 knockdown was noted to suppress colon cancer cell motility. Knockdown of LOC441461 expression suppressed the phosphorylation of MLC and LIMK1 through the inhibition of RhoA/ROCK signaling. Overall, LOC441461 was discovered to play an oncogenic role in CRC cell growth and motility through RhoA/ROCK signaling. Our findings provide new insights into the regulation of lncRNAs and their application in the treatment of colon cancer.
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http://dx.doi.org/10.3390/cancers12113171DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7692211PMC
October 2020

Linc00659, a long noncoding RNA, acts as novel oncogene in regulating cancer cell growth in colorectal cancer.

Mol Cancer 2018 03 10;17(1):72. Epub 2018 Mar 10.

Division of Colorectal Surgery, Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung, 813, Taiwan, Republic of China.

Background: Colorectal cancer (CRC) is one of the most common cancers and causes of cancer-related death worldwide. In patients with CRC, metastasis is a crucial problem that leads to treatment failure and is the primary cause of the lethality of colon cancer. Long noncoding RNAs (lncRNAs) have recently emerged as critical molecules in the development, cell growth, apoptosis, and metastasis of CRC.

Method: We investigated the transcriptome profiles of human lncRNAs in the primary tumor tissues and in the corresponding normal mucosa of two patients with CRC by using a microarray approach. The expression levels of lncRNAs were verified in colon cancer by real-time PCR. Using bioinformatics approach to illustrate putative biological function of Linc00659 in colon cancer. The effects of Linc00659 on cell growth, proliferation, cell cycle and apoptosis were studies by in vitro assays.

Results: Our data revealed that compared with adjacent normal tissues, 201 lncRNAs were deregulated (fold change ≥ 4 or ≤ 0.25) in CRC tissues. Among them, the expression levels of Linc00659 were significantly increased in colon cancer, and high expression levels were correlated with poor survival in patients with CRC. Bioinformatics analysis results indicated that Linc00659 was significantly coexpressed with cycle-related genes in CRC. Linc00659 expression knockdown could significantly suppress colon cancer cell growth by impairing cell cycle progression. In addition, our results showed that Linc00659 expression knockdown could accelerate cell apoptosis in colon cancer cells treated with chemotherapy drugs. Meanwhile, our results also demonstrated that silencing of Linc00659 expression leads to cell growth inhibition and induced apoptosis, possibly by suppressing PI3K-AKT signaling in colon cancer.

Conclusion: Linc00659 is a novel oncogenic lncRNA involved in colon cancer cell growth by modulating the cell cycle. Our findings give an insight into lncRNA regulation and provide an application for colon cancer therapy.
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http://dx.doi.org/10.1186/s12943-018-0821-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5845323PMC
March 2018

MicroRNA-324 in Human Cancer: miR-324-5p and miR-324-3p Have Distinct Biological Functions in Human Cancer.

Anticancer Res 2016 10;36(10):5189-5196

Department of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan, R.O.C.

MicroRNAs (miRNAs) are small non-coding RNAs that have crucial regulatory functions in carcinogenesis. miR-324-5p and miR-324-3p are generated from the same hairpin RNA structure, however, both are diverse in their direct target genes and expression levels. We report that expression of miR-324-5p and -3p was frequently observed to be either up-regulated or down-regulated, and the selection preference of miR-324 for 5p and 3p arms significantly varied in various types or human cancer. Overexpression of miR-324-5p or -3p suppressed growth and invasion of breast cancer cells. Overexpression of miR-324-5p reduced the growth and invasive abilities of colorectal cancer cells, whereas miR-324-3p suppressed colorectal cancer cell invasion but did not influence cell growth. We conclude that miR-324-5p and miR-324-3p might have distinct biological functions, further complicating the regulatory network in human cancer. Therefore, the arm selection preference of miR-324 may be a method for modulating its function.
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http://dx.doi.org/10.21873/anticanres.11089DOI Listing
October 2016
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