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 >

FREDERICK H. SILVER^1,2,*, TANMAY DESHMUKH²

BIOCELL, Vol.48, No.4, pp. 525-540, 2024, DOI:10.32604/biocell.2024.047965

Abstract All tissues in the body are subjected externally to gravity and internally by collagen fibril and cellular retractive forces that create stress and energy equilibrium required for homeostasis. Mechanotransduction involves mechanical work (force through a distance) and energy storage as kinetic and potential energy. This leads to changes in cell mitosis or apoptosis and the synthesis or loss of tissue components. It involves the application of energy directly to cells through integrin-mediated processes, cell-cell connections, stretching of the cell cytoplasm, and activation of the cell nucleus via yes-associated protein (YAP) and transcriptional coactivator with PDZ-motif… 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

LOKMAN VARISLI^1,2, VEYSEL TOLAN¹, JIYAN H. CEN³, SPIROS VLAHOPOULOS⁴, OSMAN CEN^5,6,*

Oncology Research, Vol.30, No.3, pp. 137-155, 2022, DOI:10.32604/or.2022.026074

Abstract Prostate cancer is one of the most often diagnosed malignancies in males and its prevalence is rising in both developed and developing countries. Androgen deprivation therapy has been used as a standard treatment approach for advanced prostate cancer for more than 80 years. The primary aim of androgen deprivation therapy is to decrease circulatory androgen and block androgen signaling. Although a partly remediation is accomplished at the beginning of treatment, some cell populations become refractory to androgen deprivation therapy and continue to metastasize. Recent evidences suggest that androgen deprivation therapy may cause cadherin switching, from More >

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 >

CLAIRE ELIZABETH HILLS, ELEFTHERIOS SIAMANTOURAS, PAUL EDWARD SQUIRES^*

BIOCELL, Vol.46, No.4, pp. 937-940, 2022, DOI:10.32604/biocell.2022.018414

Abstract Changes in cell-cell and cell-substrate adhesion markers are increasingly used to characterize disease onset and progression. However, these relationships depend on both the biochemical and molecular association between cells and between cells and their extracellular matrix, as well as the biophysical and mechanical properties orchestrated by cytoskeletal, membrane and matrix components. To fully appreciate the role of cell adhesion when determining normal physiology and the impact of disease on cellular function, it is important to consider both biochemical and biophysical attributes of the system being investigated. In this short viewpoint we reflect on our experiences 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 >