[Clinical Value of Peripheral Blood Circulating Tumor Cells Detection in Early Cervical Infiltrating Carcinoma Screening].

Objective: To observe the difference of circulating tumor cells (CTC) in peripheral blood of patients with different degrees of cervical lesions, and to evaluate the effectiveness of CTC detection in screening early invasive cervical cancer.

Methods: From December 2015 to October 2017, 63 cases of cervicitis, low-grade and high-grade intraepithelial lesions (LSIL, HSIL) and early invasive cervical cancer were confirmed by histopathological and clinical stages in Zhongshan Boai Hospital and Zhongshan Hospital Affiliated to Zhongshan University. The immunomagnetic bead negative enrichment technique combined with immunofluorescence was used.

ZBP-89 and Sp1 contribute to Bak expression in hepatocellular carcinoma cells.

Background: Kruppel family member zinc binding protein 89 (ZBP-89), also known as ZNF148, regulates Bak expression via binding to GC-rich promoter domain. It is not clear if other GC-rich binding factors, such as Sp family members, can interact with ZBPp-89 on Bak expression. This study aims to elucidate the mechanism of Bak expression regulation by ZBP-89 and Sp proteins, based on in vitro experiment and The Cancer Genome Atlas (TCGA) hepatocellular carcinoma (HCC) data cohort.

ZBP-89 reduces histone deacetylase 3 by degrading IkappaB in the presence of Pin1.

Background: Histone deacetylase 3 (HDAC3) is overexpressed in cancers and its inhibition enhances anti-tumor chemotherapy. ZBP-89, a transcription factor, can induce pro-apoptotic Bak and reduce HDAC3 but the mechanism is unknown. Pin1, a molecular switch that determines the fate of phosphoproteins, is known to interact with HDAC3.

Baicalin attenuates TNBS-induced colitis in rats by modulating the Th17/Treg paradigm.

Baicalin, a flavonoid, has a wide range of pharmacological properties, including immunomodulation. The objective of this study was to investigate the effect of baicalin on the balance of T helper 17 (Th17) and regulatory T (Treg) cells in a colitis model. The rat colitis model was induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS).

Therapeutic efficacy of improved α-fetoprotein promoter-mediated tBid delivered by folate-PEI600-cyclodextrin nanopolymer vector in hepatocellular carcinoma.

SNPs in human AFP promoter are associated with serum AFP levels in hepatocellular carcinoma (HCC), suggesting that AFP promoter variants may generate better transcriptional activities while retaining high specificity to AFP-producing cells. We sequenced human AFP promoters, cloned 15 different genotype promoters and tested their reporter activities in AFP-producing and non-producing cells. Among various AFP variant fragments tested, EA4D exhibited the highest reporter activity and thus was selected for the further study.

Epigenetic upregulation of Bak by ZBP-89 inhibits the growth of hepatocellular carcinoma.

Zinc-binding protein-89 regulates Bak to facilitate apoptosis in cancer cells. This study examined if zinc-binding protein-89 regulates Bak through an epigenetic mechanism in hepatocellular carcinoma. We first demonstrated that the expression of Bak was reduced but the levels of deoxyribonucleic acid methyltransferase 1 and histone deacetylase 3 were increased in hepatocellular carcinoma cancer tissues compared to the corresponding non-cancer tissues.

Increased glutathione and mitogen-activated protein kinase phosphorylation are involved in the induction of doxorubicin resistance in hepatocellular carcinoma cells.

Aim:   The human hepatocellular carcinoma (HCC) cell line HepG2 can easily acquire resistance to doxorubicin. However, the mechanism of action is unclear.

Methods:   In the present study, we used confocal microscopy, flow cytometry and other methods to reveal the mechanisms by which HepG2 cells acquire doxorubicin resistance.

Indomethacin and SC236 enhance the cytotoxicity of doxorubicin in human hepatocellular carcinoma cells via inhibiting P-glycoprotein and MRP1 expression.

Doxorubicin is a chemotherapeutic drug widely used for the treatment of hepatocellular carcinoma but its efficacy is restricted by multidrug resistance. Non-steroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase (COX)-2-selective inhibitors exhibit anti-cancer properties as well as abilities to overcome drug resistance. In the present study, indomethacin (a NSAID) and SC236 (a COX-2-selective inhibitor) enhanced the cytotoxicity of doxorubicin in the hepatocellular carcinoma cell line HepG2 and its drug-resistant sub-line R-HepG2.

2,3',4,4',5'-Pentamethoxy-trans-stilbene, a resveratrol derivative, inhibits colitis-associated colorectal carcinogenesis in mice.

Background And Purpose: Resveratrol, a naturally occurring polyphenolic antioxidant, has been shown to exhibit chemoprophylactic effects on cancer development. Previously, we reported that 2,3',4,4',5'-pentamethoxy-trans-stilbene (PMS), a methoxylated resveratrol derivative, exerted a highly potent anti-proliferative effect on human colon cancer cells as compared with its parent compound. In the present study, the chemopreventive effect of PMS was evaluated in a mouse model of colitis-associated colon carcinogenesis.

3,3',4,5,5'-Pentahydroxy-trans-stilbene, a resveratrol derivative, induces apoptosis in colorectal carcinoma cells via oxidative stress.

Resveratrol exhibits anti-tumor properties against different types of cancer. In this study, several polyhydroxylated resveratrol derivatives were prepared with the aim of discovering new leading compounds with clinical potential for human colon cancer chemotherapy. Among these compounds, 3,3',4,5,5'-pentahydroxy-trans-stilbene (PHS) displayed the most potent cytotoxicity and triggered apoptosis in HT-29 cells as evidenced by increased poly(ADP-ribose) polymerase (PARP) cleavage, elevated levels of cytoplasmic nucleosomes and DNA fragmentation.