An acute bleeding metastatic spinal tumor from HCC causes an acute onset of cauda equina syndrome

Wu, Chih Ying; Huang, Heng; Cho, Der Yang

doi:10.7603/s40681-015-0018-5

Cited by 14 publications

(9 citation statements)

References 13 publications

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“…The global incidence of HCC varies considerably, with particularly high rates in Southeast Asia and sub-Saharan Africa, and lower, but increasing rates, in North America and most of Europe 2 . In Taiwan, HCC is the second leading cause of cancer-related deaths 3 , 4 . Enormous studies have indicated that high percentage of HCC progress with chronic liver disease.…”

Section: Introductionmentioning

confidence: 99%

Effects of HMGB1 Polymorphisms on the Susceptibility and Progression of Hepatocellular Carcinoma

Wang¹,

Yeh²,

Lein³

et al. 2016

Int. J. Med. Sci.

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Hepatocellular carcinoma (HCC) is a malignancy of liver and a leading cause of cancer mortality worldwide. Its management is compounded by biological and clinical heterogeneity. These interindividual genetic variations can modulate the effects of HCC treatment. High-mobility group box protein 1 (HMGB1) is a well investigated, ubiquitous nuclear protein found in eukaryotic cells that plays a multiple biological roles such as DNA stability, program cell death, immune response, and furthermore in cancer progression. In this report, we examined HMGB1 single nucleotide polymorphisms (SNPs) with multiple risk factors related to HCC susceptibility and clinicopathological characteristics. Four HMGB1 SNPs (rs1412125, rs2249825, rs1045411, and rs1360485) were assessed by using a TaqMan SNPs Genotyping in 324 patients with HCC and in 695 cancer-free controls. The results showed that HMGB1 SNP rs1045411 with CT or at least one T alleles has lower risk of HCC than wild-type (CC) carriers. Moreover, HMGB1 SNP rs1412125 with TT allele has a higher risk of distant metastasis compared with patients carrying at least one C allele. The present study is the first report to discuss the risk factors associated with HMGB1 SNPs in HCC progression in Taiwan.

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Section: Introductionmentioning

confidence: 99%

Effects of HMGB1 Polymorphisms on the Susceptibility and Progression of Hepatocellular Carcinoma

Wang¹,

Yeh²,

Lein³

et al. 2016

Int. J. Med. Sci.

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“…Liver cancer is mainly a male disease, with approximately three times higher incidence and mortality among men than women. Hepatocellular carcinoma is one of the top 10 causes of cancer death worldwide (Jemal et al, 2011) and is an aggressive tumor (Wu et al, 2015). In addition, ERa was frequently found dysregulated in liver cancer and overexpression of b-catenin was observed in the nuclei of HCC patients (Lai et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Estrogen and ERα enhanced β‐catenin degradation and suppressed its downstream target genes to block the metastatic function of HA22T hepatocellular carcinoma cells via modulating GSK‐3β and β‐TrCP expression

Chen

Velmurugan

Wang

et al. 2016

Environmental Toxicology

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In our previous experiments, we found β-catenin was highly expressed in the tumor area with high invasive ability and poor prognosis. In this study, we have examined the mechanism by which ERα regulates β-catenin expression as well as the metastasis ability of hepatocellular cancer HA22T cells. To identify whether the anticancer effect of estrogen and ERα is mediated through suppression of β-catenin expression, we co-transfected pCMV-β-catenin and ERα into HA22T cells, and determined the cell motility by wound healing, invasion, and migration assays. Results showed that estrogen and/or ERα inhibited β-catenin gene expression and repressed HA22T cell motility demonstrated that similar data was observed in cells expressing the ERα stable clone. Moreover, we examined the protein-protein interaction between ERα and β-catenin by immunostain, co-immunoprecipitation, and Western blotting. E2 enhanced the binding of ERα with β-catenin and then triggered β-catenin to bind with E3 ligase (βTrCP) to promote β-catenin degradation. Finally by employing systematic ChIP studies, we showed ERα can interact directly with the β-catenin promoter region following E2 treatment. All our results reveal that estrogen and ERα blocked metastatic function of HA22T cells by modulating GSK3β and βTrCP expression and further enhanced β-catenin degradation and suppressed its downstream target genes. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 519-529, 2017.

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“…Despite improvements in surgical and medical treatments, recurrence and metastasis contributes to poor prognosis in HCC patients . Extrahepatic metastasis reportedly happens in 13.5–36.7% of cases, and HCC are known to metastasize on lungs, adrenal glands, bone marrow, and rarely on central nervous system . Therefore, understanding the molecular events and efficient targets that are involved in the survival and metastasis of HCC and to explore new therapeutically efficient factors targeting these mediators are imminent.…”

Section: Introductionmentioning

confidence: 99%

Cryptotanshinone (Dsh‐003) from Salvia miltiorrhiza Bunge inhibits prostaglandin E2‐induced survival and invasion effects in HA22T hepatocellular carcinoma cells

Chang

Lin

Shibu

et al. 2018

Environmental Toxicology

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Human hepatocellular carcinoma (HCC) is currently the second most common cancer and one of the leading causes of cancer-related mortality in Taiwan. Previous reports show that the expression of (E-type prostaglandin 2) EP2 and (E-type prostaglandin 4) EP4 are elevated in HCC and further demonstrate that Prostaglandin E2 (PGE2) induces HA22T cell proliferation and metastasis through EP2 and EP4 receptor. Danshen (root of Salvia miltiorrhiza Bunge) is a very important and popular traditional Chinese herbal medicine which is widely and successfully used against breast cancer, leukemia, pancreatic cancer, and head and neck squamous carcinoma cells. In this study, we used Cryptotansinone (Dsh-003) (MW 269.14) from Danshen to investigate their effect and corresponding mechanism of action in PGE2-treated HA22T cells. Dsh-003 inhibited HA22T cell viability and further induced cell apoptosis in PGE2-treated HA22T cells. Furthermore, Dsh-003 inhibited EP2, EP4, and their downstream effector such as p-PI3K and p-Akt expression in HA22T hepatocellular carcinoma cells. We also observed that Dsh-003 blocked PGE2-induced cell migration by down-regulating PGE2-induced β-catenin expression and by up-regulating E-cadherin and GSK3-β expression. All these findings suggest that Dsh-003 inhibit human HCC cell lines and could potentially be used as a novel drug for HCC treatment.

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An acute bleeding metastatic spinal tumor from HCC causes an acute onset of cauda equina syndrome

Cited by 14 publications

References 13 publications

Effects of HMGB1 Polymorphisms on the Susceptibility and Progression of Hepatocellular Carcinoma

Effects of HMGB1 Polymorphisms on the Susceptibility and Progression of Hepatocellular Carcinoma

Estrogen and ERα enhanced β‐catenin degradation and suppressed its downstream target genes to block the metastatic function of HA22T hepatocellular carcinoma cells via modulating GSK‐3β and β‐TrCP expression

Cryptotanshinone (Dsh‐003) from Salvia miltiorrhiza Bunge inhibits prostaglandin E2‐induced survival and invasion effects in HA22T hepatocellular carcinoma cells

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