ABSTRACT
Peliosis hepatis (PH) is a rare benign condition characterized by the presence of multiple, randomly distributed, blood filled cystic areas of variable size within the liver parenchyma. PH is difficult to recognize and may be mistaken for neoplasm, metastases or multiple abscesses. A 75-year-old female with a previous history of colon cancer was admitted when a liver mass in the right liver lobe was found 11 mo after surgery during the follow-up period. Computed tomography and magnetic resonance imaging scan of the abdomen were performed. The initial possible diagnosis was metastatic hepatocellular carcinoma. The patient underwent excision of the hepatic segment where the nodule was located. The pathological diagnosis of the surgical specimen was PH. PH should be considered in the differential diagnosis of new liver lesions in patients whose clinical settings do not clearly favor metastasization. Clinicians and radiologists must recognize these lesions to minimize the probability of misdiagnosis and inappropriate treatment.
Subject(s)
Colonic Neoplasms/pathology , Liver Neoplasms/secondary , Peliosis Hepatis/diagnosis , Aged , Biopsy , Colonic Neoplasms/surgery , Diagnosis, Differential , Diagnostic Errors , Female , Hepatectomy , Humans , Liver Neoplasms/surgery , Magnetic Resonance Imaging , Multimodal Imaging , Peliosis Hepatis/surgery , Positron-Emission Tomography , Predictive Value of Tests , Tomography, X-Ray ComputedABSTRACT
Heat shock protein 70 (Hsp70), a chaperone involved in tumor progression, is overexpressed in various human tumors. However, its role in colon cancer progression is not completely understood. In the present study, two shRNA plasmid vectors against Hsp70 were constructed and stably transfected into the colon cancer cell line HT29 to determine the effect of Hsp70 on cell proliferation, cell cycle distribution and cell apoptosis in HT29 cells in vitro, and its effect on xenograft tumor growth and apoptosis in vivo. Cell proliferation was determined using MTT assay. The results revealed that Hsp70 silencing efficiently inhibited the growth of HT29 cells in culture, induced cell cycle arrest at the G1 phase, and significantly increased apoptosis. Moreover, stable clones from the Hsp70 shRNA-2 vector suppressed xenograft tumor growth and enhanced apoptosis in vivo compared with a mock and vector control group. In conclusion, specific Hsp70 shRNA silencing may inhibit colon cancer growth, indicating that Hsp70 silencing is a potential therapeutic strategy for the treatment of colon cancer.
Subject(s)
Colonic Neoplasms/pathology , Gene Silencing , HSP110 Heat-Shock Proteins/genetics , RNA, Small Interfering/metabolism , Animals , Apoptosis , Cell Cycle , Cell Proliferation , Cell Survival , Colonic Neoplasms/genetics , Flow Cytometry , Gene Expression Regulation, Neoplastic , Gene Knockdown Techniques , Genetic Vectors/genetics , HSP110 Heat-Shock Proteins/metabolism , HT29 Cells , Humans , Mice , Mice, Nude , Transfection , Xenograft Model Antitumor AssaysABSTRACT
AIM: To investigate the effect of oncolytic adenovirus SG600-IL24 and replication-incompetent adenovirus Ad.IL-24 on hepatocellular carcinoma (HCC) cell lines and normal liver cell line. METHODS: HCC cell lines (HepG2, Hep3B and MHCC97L) and normal liver cell line (L02) with a different p53 status were infected with SG600-IL24 and Ad.IL-24, respectively. Melanoma differentiation-associated (MDA)-7/interleukin (IL)-24 mRNA and protein expressions in infected cells were detected by reverse transcription-polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA), and Western blotting, respectively. Apoptosis of HCC cells and normal liver cells was detected by cytometric assay with Hoechst33258 staining. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to investigate proliferation of HCC cells and normal liver cells, and cell cycle was assayed by flow cytometry. RESULTS: RT-PCR, ELISA and Western blotting showed that the exogenous MDA-7/IL-24 gene was highly expressed in cells infected with SG600-IL24. MTT indicated that SG600-IL24 could suppress the growth of HepG2, Hep3B, MHCC97L, with an inhibition rate of 75% ± 2.5%, 85% ± 2.0%, 72% ± 1.8%, respectively (P < 0.01), promote the apoptosis of HepG2, Hep3B, MHCC97L, with an apoptosis rate of 56.59% ± 4.0%, 78.36% ± 3.5%, 43.39% ± 2.5%, respectively (P < 0.01), and block the HCC cell lines in the G2/M phase with a blocking rate of 35.4% ± 4.2%, 47.3% ± 6.2%, 42% ± 5.0%, respectively (P < 0.01) but not the normal liver cell line in a p53-independent manner. CONCLUSION: SG600-IL24 can selectively suppress the proliferation and apoptosis of HCC cell lines in vitro but not normal liver cell line L02 in a p53-independent manner. Compared with Ad.IL-24, SG600-IL24 can significantly enhance the antitumor activity in HCC cell lines.
