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  • Open Access

    COMMENTARY

    A commentary on the interplay of biomaterials and cell adhesion: new insights in bone tissue regeneration

    A. NOEL GRAVINA1,2, NOELIA D´ELÍA1,2, LUCIANO A. BENEDINI2,3,*, PAULA MESSINA1,2

    BIOCELL, Vol.48, No.11, pp. 1517-1520, 2024, DOI:10.32604/biocell.2024.055513 - 07 November 2024

    Abstract This article navigates the relationship between biomaterials and osteogenic cell adhesion, highlighting the importance of mimicking the physiological response for bone tissue regeneration. Within this spirit is an initial description of the interaction between osteoblasts and osteoprogenitor cells with the extracellular matrix, explaining the leading role of integrins and cadherins in cell adhesion, and the intracellular signaling pathways elicited. Additionally, there is a focus on the strategies of advanced biomaterials that foster osteogenesis by replicating the native environment, taking advantage of these known specific signaling pathways. The final remarks lay on the need for careful More >

  • Open Access

    REVIEW

    Do tensile and shear forces exerted on cells influence mechanotransduction through stored energy considerations?

    FREDERICK H. SILVER1,2,*, TANMAY DESHMUKH2

    BIOCELL, Vol.48, No.4, pp. 525-540, 2024, DOI:10.32604/biocell.2024.047965 - 09 April 2024

    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 >

  • 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 - 15 November 2023

    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

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

  • Open Access

    REVIEW

    Dissecting the effects of androgen deprivation therapy on cadherin switching in advanced prostate cancer: A molecular perspective

    LOKMAN VARISLI1,2, VEYSEL TOLAN1, JIYAN H. CEN3, SPIROS VLAHOPOULOS4, OSMAN CEN5,6,*

    Oncology Research, Vol.30, No.3, pp. 137-155, 2022, DOI:10.32604/or.2022.026074 - 12 January 2023

    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 >

  • Open Access

    ARTICLE

    Cell adhesion in renal tubular epithelial cells: Biochemistry, biophysics or both

    CLAIRE ELIZABETH HILLS, ELEFTHERIOS SIAMANTOURAS, PAUL EDWARD SQUIRES*

    BIOCELL, Vol.46, No.4, pp. 937-940, 2022, DOI:10.32604/biocell.2022.018414 - 15 December 2021

    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 >

  • 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 - 28 September 2021

    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 >

  • 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 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… More >

  • Open Access

    ARTICLE

    T-box Transcription Factor Tbx3 Contributes to Human Hepatocellular Carcinoma Cell Migration and Invasion by Repressing E-Cadherin Expression

    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 >

  • Open Access

    ARTICLE

    Long Noncoding RNA NEAT1 Promotes Growth and Metastasis of Cholangiocarcinoma Cells

    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 >

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