Sann-Joong-Kuey-Jian-Tang inhibits hepatocellular carcinoma Hep-G2 cell proliferation by increasing TNF-α, Caspase-8, Caspase- 3 and Bax but by decreasing TCTP and Mcl-1 expression in vitro.

  title={Sann-Joong-Kuey-Jian-Tang inhibits hepatocellular carcinoma Hep-G2 cell proliferation by increasing TNF-$\alpha$, Caspase-8, Caspase- 3 and Bax but by decreasing TCTP and Mcl-1 expression in vitro.},
  author={Yao-Li Chen and Meng Yan and Su-Yu Chien and Shou Jen Kuo and Dar-Ren Chen and Chun-Yuan Cheng and Chin Cheng Su},
  journal={Molecular medicine reports},
  volume={7 5},
Hepatic cancer remains a challenging disease and there is a need to identify new treatments. Sann-Joong-Kuey-Jian-Tang (SJKJT), a traditional medicinal prescription, has been used to treat lymphadenopathy and exhibits cytotoxic activity in many types of human cancer cells. Our previous studies revealed that SJKJT is capable of inhibiting colon cancer colo 205 cells by inducing autophagy and apoptosis. However, the effects and molecular mechanisms of SJKJT in human hepatocellular carcinoma have… Expand
Sann-Joong-Kuey-Jian-Tang decreases the protein expression of Mcl‑1 and TCTP and increases that of TNF-α and Bax in BxPC‑3 pancreatic carcinoma cells.
It is demonstrated that SJKJT has potential as a chemotherapeutic agent for the treatment of pancreatic cancer, and inhibits the proliferation of BxPC-3 cells through the extrinsic and intrinsic pathway, inducing apoptosis in vitro. Expand
Sann-Joong-Kuey-Jian-Tang decreases the protein expression of mammalian target of rapamycin but increases microtubule associated protein II light chain 3 expression to inhibit human BxPC‑3 pancreatic carcinoma cells.
  • C. Su
  • Medicine, Biology
  • Molecular medicine reports
  • 2015
Investigation of molecular mechanisms of autophagy in human BxPC‑3 pancreatic cancer cells treated with SJKJT showed that SJkJT inhibited the proliferation of human BXPC‐3 pancreatIC cancer cells in vitro, suggesting a possible underlying molecular mechanism may be the induction of Autophagy. Expand
Sann-Joong-Kuey-Jian-Tang induces autophagy in HepG2 cells via regulation of the phosphoinositide-3 kinase/Akt/mammalian target of rapamycin and p38 mitogen-activated protein kinase pathways
Findings from the investigation of SJKJT-induced autophagy and cytotoxic mechanisms mediating these effects may assist in the development of novel chemotherapeutic agents for the treatment of malignant types of liver cancer. Expand
siRNA targeting TCTP suppresses osteosarcoma cell growth and induces apoptosis in vitro and in vivo
Results indicate that inhibition of TCTP expression exerts potential antitumor activity and may be a novel therapeutic approach in human OS. Expand
Function of myeloid cell leukaemia-1 and its regulative relations with hepatocellular carcinoma
Mcl-1 as an essential regulatory factor in HCC can be designed as target for drugs to improve the survival of HCC patients and the recent anti-hepatoma drug research and development down-regulation of M cl-1 or targeting on Mcl- 1 is discussed. Expand
Regulation of mitochondrial apoptosis by Pin1 in cancer and neurodegeneration.
The impact of Pin1 in regulating various aspects of apoptosis in different biological contexts with particular emphasis on cancer and neurodegenerative diseases is discussed. Expand
Obesity and cancer: the role of adipose tissue and adipo-cytokines-induced chronic inflammation
It is supported that inflammatory state specific of obesity may be important in obesity-cancer link and Dysfunctional adipose tissue in obesity releases a disturbed profile of adipokines with elevated levels of pro-inflammatory factors and a consequent alteration of key signaling mediators. Expand
The adipose organ and multiple myeloma: Impact of adipokines on tumor growth and potential sites for therapeutic intervention.
This review should suggest future research approaches toward developing novel treatments to target MM by targeting BMAT and its products. Expand


Sann-Joong-Kuey-Jian-Tang up-regulates the protein expression of Fas and TNF-α in colo 205 cells in vivo and in vitro.
The results demonstrate that SJKJT up-regulated Fas, TNF-α, Caspase-8 and Caspasing-3 protein expression, both in vitro and in vivo, and suggest that SJkJT has therapeutic potential in colon cancer. Expand
Sann-Joong-Kuey-Jian-Tang increases the protein expression of microtubule-associated protein II light chain 3 in human colon cancer colo 205 cells.
Findings indicate that one of the molecular mechanisms by which SJKJT inhibits the proliferation of colo 205 cells in?vitro may be through the induction of the autophagic pathway and may have therapeutic potential for the treatment of human colon cancer. Expand
San-Zhong-Kui-Jian-Tang, a traditional Chinese medicine prescription, inhibits the proliferation of human breast cancer cell by blocking cell cycle progression and inducing apoptosis.
This study suggests that the induction of p21/WAF1 and activity of the mitochondrial apoptotic system may participate in the antiproliferative activity of SZKJY in human breast cancer cells. Expand
Antiapoptotic Protein Partners Fortilin and MCL1 Independently Protect Cells from 5-Fluorouracil-induced Cytotoxicity*
Evidence is presented that fortilin and MCL1 are capable of functioning as antiapoptotic proteins independently of each other, and cytoprotective effects of these proteins together and apart in U2OS cell lines exposed to 5-FU in both monoclonal and polyclonal cell populations. Expand
TCTP protects from apoptotic cell death by antagonizing bax function
It is shown here that loss of tctp expression in mice leads to increased spontaneous apoptosis during embryogenesis and causes lethality between E6.5 and E9.5, and the antiapoptotic role of TCTP in vivo is confirmed. Expand
Regulation of proliferation, survival and apoptosis by members of the TNF superfamily.
Together these cytokines regulate cell growth/survival/apoptosis in a complex dance of changing partners and overlapping steps. Expand
Physical and Functional Interaction between Myeloid Cell Leukemia 1 Protein (MCL1) and Fortilin
Data suggest that MCL1, in addition to being an anti-apoptotic molecule, serves as a chaperone of fortilin, binding and stabilizing Fortilin in vivo, maximizing the prosurvival environment in cells. Expand
Stabilization and Enhancement of the Antiapoptotic Activity of Mcl-1 by TCTP
TCTP modulates Mcl-1's antiapoptotic activity by modulating its protein stability, and the possible mechanism(s) involved in the modulation process is discussed. Expand
An endotoxin-induced serum factor that causes necrosis of tumors.
It is proposed that TNF mediates endotoxin-induced tumor necrosis, and that it may be responsible for the suppression of transformed cells by activated macrophages. Expand
Caspases: the executioners of apoptosis.
  • G. Cohen
  • Biology, Medicine
  • The Biochemical journal
  • 1997
The importance of caspase prodomains in the regulation of apoptosis is further highlighted by the recognition of adapter molecules, such as RAIDD [receptor-interacting protein (RIP)-associated ICH-1/CED-3-homologous protein with a death domain]/CRADD (caspase and RIP adapter with death domain), which binds to the prodomain of cspase-2 and recruits it to the signalling complex. Expand