Haimei Tang

Sir Run Run Shaw Hospital, Hang-hsien, Zhejiang Sheng, China

Are you Haimei Tang?

Claim your profile

Publications (2)6.55 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Fibulin-1, a multi-functional extracellular matrix protein, has been demonstrated to be involved in many kinds of cancer, while its function in colorectal cancer (CRC) is unclear. So here we investigated the expression and function of fibulin-1 in CRC. The expression of fibulin-1 mRNA variants named A, B, C and D in human colorectal cancer cells and colorectal cancer specimens were determined by RT-PCR. Fibulin-1 protein expression in colorectal cancer and normal colorectal mucosa tissue was evaluated by western blot, and was further validated by immunohistochemistry and enzyme-linked immunosorbent assay at serum level. The correlations between fibulin-1 expression and the clinicopathological features of colorectal cancers were evaluated by Chi-square test and Fisher's exact tests. The survival rates were calculated by the Kaplan-Meier method. Among fibulin-1 A-D variants, fibulin-1D is the predominant form expressed in colorectal cancer cell lines and colorectal cancer tissue, whereas only trace amounts of fibulin-1A-C were detectable. Fibulin-1 expressed higher in the CRC tissues and serum compared to normal control. So in the process of tumorigenesis of CRC, fibulin-1 is upregulated, however, high fibulin-1 expression showed longer survival time in colorectal cancer patients, especially in the patients with stage I/II. Low fibulin-1 expression was significantly associated with lymph node involvement, distant metastasis and Dukes' C and D stage (P < 0.05 for each). Fibulin-1 protein expression may be useful as a diagnosis and prognosis marker for colorectal cancer.
    American Journal of Translational Research 01/2015; 7(2):339-47. · 3.23 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Targeting the ubiquitin-proteasome pathway is a promising approach for anticancer strategies. Recently, we found Bik accumulation in cancer cell lines after they were treated with bortezomib. However, recent evidence indicates that proteasome inhibitors may also induce the accumulation of anti-apoptotic Bcl-2 family members. The current study was designed to analyze the levels of several anti-apoptotic members of Bcl-2 family in different human cancer cell lines after they were treated with proteasome inhibitors. Different human cancer cell lines were treated with proteasome inhibitors. Western blot were used to investigate the expression of Mcl-1 and activation of mitochondrial apoptotic signaling. Cell viability was investigated using SRB assay, and induction of apoptosis was measured using flow cytometry. We found elevated Mcl-1 level in human colon cancer cell lines DLD1, LOVO, SW620, and HCT116; human ovarian cancer cell line SKOV3; and human lung cancer cell line H1299, but not in human breast cancer cell line MCF7 after they were treated with bortezomib. This dramatic Mcl-1 accumulation was also observed when cells were treated with other two proteasome inhibitors, MG132 and calpain inhibitor I (ALLN). Moreover, our results showed Mcl-1 accumulation was caused by stabilization of the protein against degradation. Reducing Mcl-1 accumulation by Mcl-1 siRNA reduced Mcl-1 accumulation and enhanced proteasome inhibitor-induced cell death and apoptosis, as evidenced by the increased cleavage of caspase-9, caspase-3, and poly (ADP-ribose) polymerase. Our results showed that it was not only Bik but also Mcl-1 accumulation during the treatment of proteasome inhibitors, and combining proteasome inhibitors with Mcl-1 siRNA would enhance the ultimate anticancer effect suggesting this combination might be a more effective strategy for cancer therapy.
    BMC Cancer 11/2011; 11(1):485. DOI:10.1186/1471-2407-11-485 · 3.32 Impact Factor