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Search Results (4)
  • Open Access

    ARTICLE

    ELK3-ID4 axis governs the metastatic features of triple negative breast cancer

    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 between the expression of ELK3… More > Graphic Abstract

    ELK3-ID4 axis governs the metastatic features of triple negative breast cancer

  • Open Access

    ARTICLE

    miR-186 Suppresses the Progression of Cholangiocarcinoma Cells Through Inhibition of Twist1

    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 direct target of miR-186. Further,… More >

  • Open Access

    REVIEW

    Metformin and colorectal cancer

    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, many of these results were… More >

  • Open Access

    ABSTRACT

    Oscillatory Shear Stress Induces Endothelial Dysfunction through the Activation of P2Y12

    Jianxiong Xu1, Lu Wang1, Jinxuan Wang1, Juhui Qiu1,*, Guixue Wang1,*

    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 in endothelial cells of atheroprone… More >

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