Tissue Microarray Immunohistochemical Profiles of p53 and pRB in Hepatocellular Carcinoma and Hepatoblastoma

Azlin, Abdul Hadi; Looi, Lai‐Meng; Cheah, Phaik Leng

doi:10.7314/apjcp.2014.15.9.3959

Cited by 9 publications

(8 citation statements)

References 24 publications

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“…The immunostaining detection and the staining patterns of p53, bcl2, HER2, E-cadherin and Ki67 in our breast cancer TmA were studied in cancer cells and stroma as well as in cytoplasm and nuclei; and semi-quantitatively represented as previously reported (Elkablawy et al, 2001;Wolff et al, 2007;Rakhshani et al, 2014). The results were in concordance with previously published data regarding immunostaining expression of p53, bcl2, HER2, E-cadherin and Ki67 in tissue microarrays (Cass et al, 2012;Laurinavicius et al, 2012;Syed et al, 2013;Azlin et al, 2014). Also, the results obtained with SISH for measuring HER2 amplification in the current study were consistent with those of other studies using SISH for HER2 assay (Papouchado et al, 2010;Wolff et al, 2013).…”

Section: Discussionsupporting

confidence: 91%

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High Quality Tissue Miniarray Technique Using a Conventional TV/Radio Telescopic Antenna

Elkablawy

Albasri²

2015

Asian Pacific Journal of Cancer Prevention

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Jawhar, 2009). It has greatly facilitated the in situ analysis of molecular targets at the DNA, mRNA, and protein levels under standardized conditions in a large number of archived pathology specimens (Fowler et al., 2011).Advances of the technique enables pathologists to perform large-scale analyses using immunohistochemistry, fluorescence in situ hybridization (FISH), or RNA in situ hybridization (ISH) at substantially faster and markedly lower costs compared with conventional approaches

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Section: Discussionsupporting

confidence: 91%

“…Mohamed A Elkablawy 1,2 *, Abdulkader M Albasri 2 2012; Syed et al, 2013;Azlin et al, 2014;Rakhshani et al, 2014). Several efforts have been made by many researchers in the last 15 years, to develop and improve the output of the TMA technique.…”

Section: High Quality Tissue Miniarray Technique Using a Conventional Tv/radio Telescopic Antennamentioning

confidence: 99%

High Quality Tissue Miniarray Technique Using a Conventional TV/Radio Telescopic Antenna

Elkablawy

Albasri²

2015

Asian Pacific Journal of Cancer Prevention

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“…Liver cancer is one of the most common tumor types, is the third leading cause of cancer-associated mortality worldwide, and consists of hepatocellular carcinoma (HCC) and hepatoblastoma (HB) (1). HCC and HB have distinct cytological characteristics (2). HepG2 was originally thought to be a HCC cell line; however, was misidentified and has subsequently been demonstrated to be derived from hepatoblastoma (3).…”

Section: Introductionmentioning

confidence: 99%

miR‑30a‑3p inhibits the proliferation of liver cancer cells by targeting DNMT3a through the PI3K/AKT signaling pathway

Chen

Gao

et al. 2019

Oncol Lett

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MicroRNAs (miRNAs or miRs) are crucial for normal development and maintenance of homeostasis. Dysregulated miRNA expression contributes to numerous pathological conditions, including cancer tumorigenesis. However, a limited number of studies have examined the regulatory effects of miR-30a-3p in tumorigenesis. Therefore, the present study investigated the mechanistic process of tumorigenesis in liver cancer. The results revealed a high expression of DNA methyltransferase 3a (DNMT3a) and a low expression of miR-30a-3p in HepG2 cells compared with that in the L02 cell line. A luciferase reporter assay demonstrated that DNMT3a is a direct target of miR-30a-3p. In addition, DNMT3a overexpression significantly enhanced cell proliferation, which was reversed by a miR-30a-3p mimic. Similarly, the miR-30a-3p mimic blocked DNMT3a-triggered cell cycle processes and apoptosis by attenuating active p-AKT and p-PI3K in HepG2 cells. In summary, the results of the present study demonstrate that miR-30a-3p is essential for cell proliferation regulation via its association with AKT/PI3K signaling in liver cancer. These results provide insight into the molecular mechanism by which miR-30a-3p inhibits liver cancer cell proliferation and provides a foundation for its clinical development and application.

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“…It is known that metformin stops the propagation of breast cancer cells and this is not associated with p53 expression (Zhuang and Miskimins, 2008a). Results obtained using the HCC cell line suggests that the cytotoxic mechanism of metformin action is independent of p53 (Chen et al, 2013;Azlin et al, 2014). It can't be excluded that may also be the result of stimulation of poly-ADP-ribose polymerase synthesis by metformin (Chen et al, 2013).…”

Section: Discussionmentioning

confidence: 98%

Effects of Epothilone A in Combination with the Antidiabetic Drugs Metformin and Sitagliptin in HepG2 Human Hepatocellular Cancer Cells: Role of Transcriptional Factors NF-κB and p53

Rogalska¹,

Śliwińska²,

Kasznicki³

et al. 2016

Asian Pacific Journal of Cancer Prevention

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Type 2 diabetes mellitus patients are at increased risk of many forms of malignancies, especially of the pancreas, colon and hepatocellular cancer. Unfortunately, little is known of the possible interaction between antidiabetic drugs and anticancer agents. The present study investigates the influence of metformin (MET) and sitagliptin (SITA) on the in vitro anticancer activity of the microtubule depolymerization inhibitor agent epothilone A (EpoA). Hepatocellular liver carcinoma cell line (HepG2) viability and apoptosis were determined by the MTT test and by double staining with PO-PRO-1 and 7-aminoactinomycin D, respectively, after treatment with EpoA, metformin or sitagliptin. The levels of nuclear factor NF-κB and p53 were evaluated in the presence and absence of inhibitors. While EpoA and MET inhibited HepG2 cell proliferation, SITA did not. EpoA and SITA induced higher p53 levels than MET. All tested drugs increased the level of NF-κB. Only MET enhanced the proapoptotic effect of EpoA. The EpoA+MET combination evoked the highest cytotoxic effect on HepG2 cells and led to apoptosis independent of p53, decreasing the level of NF-κB. These findings support the link between NF-κB and p53 in the modulation of apoptotic effects in HepG2 cells treated by EpoA. Our studies indicate that the combination of EpoA and MET applied in subtoxic doses has a stronger cytotoxic effect on liver cancer cells than each of the compounds alone. The therapeutic advantages of the combination of EpoA with MET may be valuable in the treatment of patients with diabetes mellitus type 2 (T2DM) and liver cancer.

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Tissue Microarray Immunohistochemical Profiles of p53 and pRB in Hepatocellular Carcinoma and Hepatoblastoma

Cited by 9 publications

References 24 publications

High Quality Tissue Miniarray Technique Using a Conventional TV/Radio Telescopic Antenna

High Quality Tissue Miniarray Technique Using a Conventional TV/Radio Telescopic Antenna

miR‑30a‑3p inhibits the proliferation of liver cancer cells by targeting DNMT3a through the PI3K/AKT signaling pathway

Effects of Epothilone A in Combination with the Antidiabetic Drugs Metformin and Sitagliptin in HepG2 Human Hepatocellular Cancer Cells: Role of Transcriptional Factors NF-κB and p53

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