Ruoyu Wang^*†, Heming Li^†, Xuefen Guo^†, Zhe Wang^†, Shanshan Liang^†, Chengxue Dang^*

Oncology Research, Vol.24, No.4, pp. 225-231, 2016, DOI:10.3727/096504016X14648701447931

Abstract Recurrence and distant metastasis are the most common cause of therapeutic failure in nasopharyngeal carcinoma (NPC) patients. Insulin-like growth factor I (IGF-I) can induce epithelial-to-mesenchymal transition (EMT) in many epithelial tumors; however, whether IGF-I can enhance NPC metastasis by EMT and the mechanisms remain unclear. Herein, we have identified that IGF-I could induce EMT and enhance migration ability in NPC cell lines. Furthermore, both Src inhibitor and microRNA-30a (miR-30a) inhibitor reversed IGF-I-induced EMT, suggesting the involvement of an IGF-IR–Src–miR-30a–E-cadherin pathway in IGF-Iinduced EMT in NPC cell lines. Overall, the results of the present study may More >

Qian Li, Jing Jin, Jianghui Liu, Liqun Wang, Yutong He

Oncology Research, Vol.24, No.3, pp. 205-214, 2016, DOI:10.3727/096504016X14648701447896

Abstract We recently found that SLC39A5 (ZIP5), a zinc transporter, is overexpressed in esophageal cancer. Downregulation of ZIP5 inhibited the proliferation, migration, and invasion of the esophageal cancer cell line KYSE170 in vitro. In this study, we found that downregulation of SLC39A5 (ZIP5) by interference resulted in a significant reduction in esophageal cancer tumor volume and weight in vivo. COX2 (cyclooxygenase 2) expression was decreased and E-cadherin expression was increased in the KYSE170K xenografts, which was caused by the downregulation of ZIP5. However, we did not find that the downregulation of ZIP5 caused a change in More >

Xianguang Feng^*, Wenhuan Yao^†, Zengzhen Zhang^*, Fangshui Yuan^*, Li Liang^*, Jingqiang Zhou^*, Shuang Liu^*, Jiqing Song^‡

Oncology Research, Vol.26, No.6, pp. 959-966, 2018, DOI:10.3727/096504017X15145624664031

Abstract Tbx3, a member of the T-box family of transcription factors, contributes directly to tumor formation, migration, and invasion. However, the role of Tbx3 in the metastasis of HCC remains unclear. In the present study, Tbx3 expression was detected in HCC tissues and cells by Western blot, and Tbx3 expression was regulated by use of siRNAs or lentivirus-mediated vectors. Here we found that Tbx3 protein expression increased in HCC tissues and cell lines. Tbx3 expression was positively associated with multiple tumor nodes, venous infiltration, and advanced TNM tumor stage. Survival analysis demonstrated that Tbx3 expression was… More >

Cheng Zhang^*, Jing-Yi Li^*, Fu-Zhou Tian^†, Gang Zhao^‡, Hai Hu^‡, Yue-Feng Ma^*, Yu-Long Yang^*

Oncology Research, Vol.26, No.6, pp. 879-888, 2018, DOI:10.3727/096504017X15024935181289

Abstract Long noncoding RNAs (lncRNAs) are known to play important roles in cancers. However, little is known about lncRNAs in cholangiocarcinoma (CCA), a cholangiocyte malignancy with poor prognosis. We investigated the role of nuclear paraspeckle assembly transcript 1 (NEAT1) lncRNA in promoting CCA. qRT-PCR analysis of patient samples showed that NEAT1 expression was higher in CCA tumors than in matched adjacent nontumor tissue. NEAT1 levels were also higher in CCA cell lines than in a normal biliary epithelium cell line (HIBEpic). NEAT1 knockdown in CCA cell lines using shNEAT1 reduced cell proliferation and colony formation in… More >

JIN-HO CHOI, JOO DONG PARK, SEUNG HEE CHOI, EUN-SU KO, HYE JUNG JANG, KYUNG-SOON PARK^*

Oncology Research, Vol.32, No.1, pp. 127-138, 2024, DOI:10.32604/or.2023.042945

Abstract Purpose: Cancer cell metastasis is a multistep process, and the mechanism underlying extravasation remains unclear. ELK3 is a transcription factor that plays a crucial role in regulating various cellular processes, including cancer metastasis. Based on the finding that ELK3 promotes the metastasis of triple-negative breast cancer (TNBC), we investigated whether ELK3 regulates the extravasation of TNBC by forming the ELK3-ID4 axis. ID4 functions as a transcriptional regulator that interacts with other transcription factors, inhibiting their activity and subsequently influencing various biological processes associated with cell differentiation, survival, growth, and metastasis. Methods: We assessed the correlation… More > Graphic Abstract

Ming Zhang, Baochang Shi, Kai Zhang

Oncology Research, Vol.27, No.9, pp. 1061-1068, 2019, DOI:10.3727/096504019X15565325878380

Abstract Deregulation of miR-186 and Twist1 has been identified to be involved in the progression of multiple cancers. However, the detailed molecular mechanisms underlying miR-186-involved cholangiocarcinoma (CCA) are still unknown. In this study, we found that miR-186 was downregulated in CCA tissues and cell lines, and negatively correlated with the expression of Twist1 protein. In vitro assays demonstrated that miR-186 mimics repressed cell proliferation, in vivo tumor formation, and caused cell cycle arrest. miR-186 mimics also inhibited the migration and invasion of CCLP1 and SG-231 cells. Mechanistically, the 3′-untranslated region (3′-UTR) of Twist1 mRNA is a More >

GASTÓN AMABLE^#, EDUARDO MARTÍNEZ-LEÓN^#, MARÍA E. PICCO, OSVALDO REY

BIOCELL, Vol.46, No.1, pp. 51-59, 2022, DOI:10.32604/biocell.2022.017565

Abstract Colorectal cancer (CRC) is one of the main causes of cancer-related mortality in the developed world despite recent developments in detection and treatment. Several epidemiological studies indicate that metformin, a widely prescribed antidiabetic drug, exerts a protective effect on different cancers including CRC. Furthermore, a recent double-blind placebo-controlled, randomized trial showed that metformin significantly decreased colorectal adenoma recurrence. Studies exploring the mechanism of action of metformin in cells derived from different types of cancers reported many effects including respiratory chain complex 1 inhibition, Akt phosphorylation inhibition, ATP depletion, PKA activation and Wnt signaling inhibition. However, More >

Jianxiong Xu¹, Lu Wang¹, Jinxuan Wang¹, Juhui Qiu^1,*, Guixue Wang^1,*

Molecular & Cellular Biomechanics, Vol.16, Suppl.2, pp. 142-142, 2019, DOI:10.32604/mcb.2019.07273

Abstract Endothelial cell injured or dysfunction, which results lipid deposition and inflammation, is the key point to exacerbate the process of atherosclerosis [1, 2]. Meanwhile oscillatory shear stress is a key factor that results cell dysfunction in vascular disease [3, 4]. Previous research reported that P2Y12 plays a critical role in the development of atherosclerotic lesion through promoting smooth muscle cells migration [5]. As well P2Y12 stimulated the internalization and transendothelial transport of high density lipid. However, whether the P2Y12 induce atherosclerosis through endothelial cell remain elusive. In this study we firstly found P2Y12 were expressed… More >