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  • Open Access


    Gastrin Enhances Autophagy and Promotes Gastric Carcinoma Proliferation via Inducing AMPKα

    Zhuang Kun*†, Guo Hanqing*, Tang Hailing*, Yan Yuan*, Zhang Jun, Zhang Lingxia*, Han Kun*, Zhang Xin*

    Oncology Research, Vol.25, No.8, pp. 1399-1407, 2017, DOI:10.3727/096504016X14823648620870

    Abstract Gastric cancer (GC) is one of the most frequent epithelial malignancies worldwide. The gastrointestinal (GI) peptide gastrin is an important regulator of the secretion and release of gastric acid from stomach parietal cells, and it also plays a vital role in the development and progression of GC. The aim of the current study was to investigate the role and underlying mechanism of gastrin and autophagy in regulating GC tumorigenesis. Gastrin-17 amide (G-17) was applied in the GC cell lines SGC7901 and MGC-803. The results showed that G-17 maintained the high viability of SGC7901 and MGC-803.… More >

  • Open Access


    miR-101-3p Suppresses HOX Transcript Antisense RNA (HOTAIR)-Induced Proliferation and Invasion Through Directly Targeting SRF in Gastric Carcinoma Cells

    Xiaoyu Wu*1, Jin Zhou†1, Zhenfeng Wu*, Che Chen*, Jiayun Liu*, Guannan Wu*, Jing Zhai*, Fukun Liu*, Gang Li

    Oncology Research, Vol.25, No.8, pp. 1383-1390, 2017, DOI:10.3727/096504017X14879366402279

    Abstract miR-101-3p has been identified as a tumor suppressor in several cancers, but its exact role in gastric adenocarcinoma is still largely unknown. In this study, we found that, compared with the RGM-1 human normal gastric epithelial cells, miR-101-3p was significantly downregulated in all six human gastric adenocarcinoma cell lines, including BGC-823, MNK-45, MGC-803, SGC-7901, AGS, and HGC-27. Overexpression of miR- 101-3p suppressed both the proliferation and invasion of AGS gastric adenocarcinoma cells, and knockdown of miR-101-3p displayed the opposite effect. In addition, miR-101-3p could directly target and suppress the expression of the serum response factor More >

  • Open Access


    MicroRNA-221-3p Plays an Oncogenic Role in Gastric Carcinoma by Inhibiting PTEN Expression

    Jianping Shi*1, Yi Zhang†1, Nuyun Jin*, Yuqin Li*, Shengtian Wu*, Leiming Xu

    Oncology Research, Vol.25, No.4, pp. 523-536, 2017, DOI:10.3727/096504016X14756282819385

    Abstract Gastric carcinoma is one of the most common malignancies in men, and microRNA plays a critical role in regulating the signaling networks of gastric carcinoma tumorigenesis and metastasis. We first report the functional characteristics of miR-221-3p in gastric carcinoma. Quantification in gastric carcinoma cell lines and tumor samples reveals significantly increasing miR-221-3p expression. Moreover, a high level of miR-221-3p is correlated with a poor prognosis for gastric carcinoma patients. Ectopic miR-221-3p expression significantly promotes gastric carcinoma cell proliferation, invasion, and sphere formation, while silencing miR- 221-3p significantly inhibits these abilities in gastric carcinoma cells. Tests More >

  • Open Access


    Long Noncoding RNA CAT104 Promotes Cell Viability, Migration, and Invasion in Gastric Carcinoma Cells Through Activation of MicroRNA-381-Inhibiting Zinc Finger E-box-Binding Homeobox 1 (ZEB1) Expression

    Gang Yuan, Jingzi Quan, Dongfang Dong, Qunying Wang

    Oncology Research, Vol.26, No.7, pp. 1037-1046, 2018, DOI:10.3727/096504017X15144748428127

    Abstract Gastric carcinoma (GC) remains the second leading cause of cancer-related deaths worldwide. Good biomarkers are of paramount importance for GC therapy. This study aimed to assess the role of long noncoding RNA (lncRNA) CAT104 in GC. We found that CAT104 was highly expressed in human GC NCI-N87, SGC7901, BGC823, BGC803, and AGS cells. Suppression of CAT104 decreased NCI-N87 cell viability, migration, and invasion, but promoted apoptosis. CAT104 knockdown enhanced the expression of microRNA- 381 (miR-381) expression in NCI-N87 cells. miR-381 participated in the regulatory effects of CAT104 on NCI-N87 cell viability, migration, invasion, and apoptosis. More >

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