XINFENG ZHANG^1,2,#, SHUANG LI^2,#, MEIRU SONG^1,2, YUE CHEN³, LIANGZHENG CHANG³, ZHERUI LIU⁴, HONGYUAN DAI³, YUTAO WANG⁴, GANGQI YANG³, YUN JIANG^5,6,*, YINYING LU^1,2,*

Oncology Research, Vol.32, No.4, pp. 679-690, 2024, DOI:10.32604/or.2024.046231 - 20 March 2024

Abstract Liver cancer is a prevalent malignant cancer, ranking third in terms of mortality rate. Metastasis and recurrence primarily contribute to the high mortality rate of liver cancer. Hepatocellular carcinoma (HCC) has low expression of focal adhesion kinase (FAK), which increases the risk of metastasis and recurrence. Nevertheless, the efficacy of FAK phosphorylation inhibitors is currently limited. Thus, investigating the mechanisms by which FAK affects HCC metastasis to develop targeted therapies for FAK may present a novel strategy to inhibit HCC metastasis. This study examined the correlation between FAK expression and the prognosis of HCC. Additionally,… More >

Nan Zhu¹, Mahui Si¹, Ning Yang, Yingying Jing, Yong Fu, Xijun Zhao, Zhipeng Lin, Guangshun Yang

Oncology Research, Vol.25, No.6, pp. 1001-1008, 2017, DOI:10.3727/096504016X14796039599926

Abstract Ras-association domain family 6 (RASSF6), a member of the RASSF family, is frequently downregulated in various types of cancer. However, the roles of RASSF6 in human hepatocellular carcinoma (HCC) are still unclear. In this study, we investigated the biological functions and related molecular mechanisms in HCC. Our results found that RASSF6 is expressed in low amounts in HCC tissues and cell lines. Overexpression of RASSF6 obviously inhibited the proliferation, invasion, and EMT process in HCC cells. Furthermore, overexpression of RASFF6 greatly downregulated the protein levels of phosphorylated focal adhesion kinase (FAK), MMP-2, and MMP-9 in More >

Donald F. Ward Jr.^*, William A. Williams^*, Nicole E. Schapiro^*, Samuel R. Christy^*, Genevieve L. Weber^*, Megan Salt, Robert F. Klees^*, Adele Boskey^†, George E. Plopper ^∗,‡

Molecular & Cellular Biomechanics, Vol.4, No.4, pp. 177-188, 2007, DOI:10.3970/mcb.2007.004.177

Abstract Focal adhesion kinase (FAK) is a key integrator of integrin-mediated signals from the extracellular matrix to the cytoskeleton and downstream signaling molecules. FAK is activated by phosphorylation at specific tyrosine residues, which then stimulate downstream signaling including the ERK1/2 pathway, leading to a variety of cellular responses. In this study, we examined the effects of FAK point mutations at tyrosine residues (Y397, Y925, Y861, and Y576/7) on osteogenic differentiation of human mesenchymal stem cells exposed to collagen I and cyclic tensile strain. Our results demonstrate that FAK signaling emanating from Y397, Y925, and to a More >

E. Takai¹, R. Landesberg², R.W. Katz², C.T. Hung³, X.E Guo^1,4

Molecular & Cellular Biomechanics, Vol.3, No.1, pp. 1-12, 2006, DOI:10.3970/mcb.2006.003.001

Abstract Osteoblast interactions with extracellular matrix (ECM) proteins are known to influence many cell functions, which may ultimately affect osseointegration of implants with the host bone tissue. Some adhesion-mediated events include activation of focal adhesion kinase, and subsequent changes in the cytoskeleton and cell morphology, which may lead to changes in adhesion strength and cell responsiveness to mechanical stimuli. In this study we examined focal adhesion kinase activation (FAK), F-actin cytoskeleton reorganization, adhesion strength, and osteoblast responsiveness to fluid shear when adhered to type I collagen (ColI), glass, poly-L-lysine (PLL), fibronectin (FN), vitronectin (VN), and serum… More >

T.H. Satoh², T.A. Surmacz³, O. Nyormoi⁴, C.M. Whitacre¹

BIOCELL, Vol.27, No.1, pp. 47-55, 2003, DOI:10.32604/biocell.2003.27.047

Abstract This study shows a strong association between cell attachment to substratum and activation of β1-integrin-signaling with resistance to the camptothecin derivative topotecan (TPT) in breast cancer cells. We propose a mechanistic-driven approach to sensitize the cells to camptothecins. ZR-75-1 anchoragedependent breast cancer cell line, its derivative 9D3S suspension cells (9D3S-S), and 9D3S cells attached to fibronectin-coated plates (9D3S-A) were treated with TPT (1 µM) or CPT-11 (40 µM) for 48 h. Programmed cell death (PCD), as shown by poly(ADP-ribose) polymerase (PARP), pro-caspase-3 and pro-caspase-9 cleavage, was observed in 9D3S-S cells but not in ZR-75-1 or More >