Deleted in liver cancer 1 expression and localization in hepatocellular carcinoma tissue sections

August 2014
Oncology Letters;2014, Vol. 8 Issue 2, p785
Academic Journal
The deleted in liver cancer (DLC) protein family is composed of proteins that are hypothesized to function predominantly by regulating the activity of the small GTPases. The aim of the present study was to determine the expression and exact localization of DLC1 in hepatocellular carcinoma (HCC) tissue sections. In two types of HCC tissues, typical and fibrolamellar, immunohistochemical and immunofluorescent analysis were performed to assess DLC1 immunoreactivity. Additionally, the DLC1 gene status was determined by the fluorescence in situ hybridization. According to the observations, DLC1 is often lost in cancer cells; however, it can remain within the stromal component of tumor sections. The DLC1 immunoreactivity was particularly noticeable within the capsules surrounding the tumor masses. It was found that the DLC1 gene was deleted in 52% of HCC cases. In addition, the hemizygous deletion was observed to be independent of the HCC subtype. The results indicate that although the loss of DLC1 is a common step during hepatocarcinogenesis, this protein may be present in the tumor microenvironment.


Related Articles

  • MicroRNA-205 regulates ubiquitin specific peptidase 7 protein expression in hepatocellular carcinoma cells. LIANG ZHU; RONG LIU; WEI ZHANG; SHENG QIAN; JIAN-HUA WANG // Molecular Medicine Reports;2015, Vol. 12 Issue 3, p4652 

    Ubiquitin specific peptidase 7 (UPS7) has a critical role in the development and progression of cancer, at least in part, through its regulation of p53 protein stability. However, its molecular determinants remain to be elucidated. In the present study, it was identified that microRNA-205...

  • An essential part for Rho?associated kinase in the transcellular invasion of tumor cells. Itoh, Kazuyuki; Yoshioka, Kiyoko; Akedo, Hitoshi; Uehata, Masayoshi; Ishizaki, Toshimasa; Narumiya, Shuh // Nature Medicine;Feb1999, Vol. 5 Issue 2, p221 

    Adhesion of tumor cells to host cell layers and subsequent transcellular migration are pivotal steps in cancer invasion and metastasis. The small GTPase Rho controls cell adhesion and motility through reorganization of the actin cytoskeleton and regulation of actomyosin contractility. Cultured...

  • The small GTPase Rab29 is a common regulator of immune synapse assembly and ciliogenesis. Onnis, A; Finetti, F; Patrussi, L; Gottardo, M; Cassioli, C; Spanò, S; Baldari, C T // Cell Death & Differentiation;Oct2015, Vol. 22 Issue 10, p1687 

    Accumulating evidence underscores the T-cell immune synapse (IS) as a site of intense vesicular trafficking, on which productive signaling and cell activation crucially depend. Although the T-cell antigen receptor (TCR) is known to exploit recycling to accumulate to the IS, the specific pathway...

  • Inhibition of hepatocellular carcinoma by fulvestrant involves the estrogen receptor α and Wnt pathways in vitro and in patients. CONG-JUN WANG; DE-KAI GUO; TIAN-GENG YOU; DONG-WEI SHEN; CHAO WANG; LIN TANG; JIAN WANG; RONG-HUA XU; HUI ZHANG // Molecular Medicine Reports;2014, Vol. 10 Issue 6, p3125 

    The aim of the present study was to investigate the effect of anti-estrogen treatment (fulvestrant) on the biological activity of hepatocellular carcinoma (HCC), involving the estrogen receptor α (ERα) and Wnt pathways, and to evaluate whether ERα and Wnt inhibitory factor-1 (WIF1)...

  • Twists and turns of invasion. Childs, Geoffrey; Segall, Jeffrey E. // Nature Cell Biology;Apr2012, Vol. 14 Issue 4, p337 

    The transcription factor Twist1 is overexpressed in tumours and can induce the epithelial-mesenchymal transition, resulting in increased invasiveness. Twist1 is now shown to regulate cancer cell migration and invasion in three-dimensional environments by activating the RAC1 GTPase through...

  • A Trio-Rac1-Pak1 signalling axis drives invadopodia disassembly. Moshfegh, Yasmin; Bravo-Cordero, Jose Javier; Miskolci, Veronika; Condeelis, John; Hodgson, Louis // Nature Cell Biology;Jun2014, Vol. 16 Issue 6, p574 

    Rho family GTPases control cell migration and participate in the regulation of cancer metastasis. Invadopodia, associated with invasive tumour cells, are crucial for cellular invasion and metastasis. To study Rac1 GTPase in invadopodia dynamics, we developed a genetically encoded, single-chain...

  • Regulation of collective cell migration by RhoGAP myosin IXA. Omelchenko, Tatiana // Small GTPases;2012, Vol. 3 Issue 4, Special section p1 

    Collective cell migration is a key process during epithelial morphogenesis, tissue regeneration and tumor dissemination. During collective epithelial migration, anterior-posterior polarity, apical-basal polarity and cell-cell junctions must be dynamically coordinated, but the underlying...

  • BART Inhibits Pancreatic Cancer Cell Invasion by Rac1 Inactivation through Direct Binding to Active Rac1. Taniuchi, Keisuke; Yokotani, Kunihiko; Saibara, Toshiji // Neoplasia;May2012, Vol. 14 Issue 5, p440 

    We report that Binder of Arl Two (BART) plays a role in inhibiting cell invasion by regulating the activity of the Rho small guanosine triphosphatase protein Rac1 in pancreatic cancer cells. BART was originally identified as a binding partner of ADP-ribosylation factor-like 2, a small G protein...

  • RLIP76 is overexpressed in human glioblastomas and is required for proliferation, tumorigenesis and suppression of apoptosis. Wang, Qi; Wang, Jun-Yu; Zhang, Xiao-Ping; Lv, Zhong-Wei; Fu, Da; Lu, Yi-Cheng; Hu, Guo-Han; Luo, Chun; Chen, Ju-Xiang // Carcinogenesis;Apr2013, Vol. 34 Issue 4, p916 

    The guanosine triphosphatase-activating protein RLIP76 is overexpressed in many malignant tumor cells, but it is unclear if RLIP76 overexpression contributes to the high proliferative potential of glioma cells. We demonstrate that RLIP76 messenger RNA and protein expression are positively...


Read the Article


Sorry, but this item is not currently available from your library.

Try another library?
Sign out of this library

Other Topics