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Latexin is downregulated in several types of human cancer. There turned out to be a relation between latexin expression and HCC (Hepatocellular carcinoma). The role of latexin in the regulation of the proliferation of HCC-derived cells was investigated both in vitro and in vivo. Results revealed that overexpression of latexin inhibited SK-hep-1 and HepG2 cellular colony formation and tumor growth. Latexin overexpression promoted cell cycle arrest in the G0/G1 phase in SK-hep-1 and silencing of latexin promoted the cell cycle transition from G0/G1 phase to S phase in YY-8103. The cyclin-dependent kinase inhibitors (CDKIs), cyclin D1 and cyclin E were shown to be differentially expressed in latexin-overexpressed cells and latexin-silenced cells. These results indicated that latexin may be an effective target for gene therapy.
Existing evidence suggested that latexin also has a strong connection with pancreatic cancer containing cancer stem cells (CSCs), which may be relevant to the resistance of chemotherapy. Latexin is a negative regulator of stem cell proliferation. Latexin protein and mRNA expression levels in CD133+ miapaca-2 cells were significantly lower than those in CD133- cells. Latexin-treated CD133+ exhibited increased apoptosis and low proliferation activity, down-regulation of Bcl-2 and up-regulation of Bax expression in a dose-dependent manner. Thus it was concluded that Latexin induced apoptosis and inhibited the proliferation of CD133+ miapaca-2 cells. These changes are associated with down-regulation of Bcl-2 and up-regulation of Bax.
Latexin was also proved to be connected with docetaxel (DOX), the standard of care for advanced (PCa). Analysis from the PC-3 PCa (prostate cancer) cell line and its DOX-resistant derivative (PC3-TxR) revealed that the expression of latexin in the resistant cells decreased. Latexin expression was inversely correlated with taxane resistance in a panel of PCa cell lines. Latexin knockdown conferred DOX resistance to PCa cells in vitro and in vivo, while latexin overexpression reduced DOX resistance in several PCa cell lines. It was identified that bone stromal cells decreased latexin expression through methylation and induced chemoresistance in PCa in vitro. These findings revealed that a subset of PCa develops DOX resistance through loss of latexin expression associated with methylation and that the bone microenvironment promotes this drug resistance phenotype. This study suggested that the latexin pathway should be further explored as a viable target for preventing or reversing taxane resistance in PCa.
There has also been a connection between latexin hematological malignancies. Latexin is a negative regulator of hematopoietic stem cell number. Its dysregulated expression in other tumors led researchers to hypothesize that latexin may have tumor suppressor properties in hematological malignancies. It was found that latexin was down-regulated in a variety of leukemia and lymphoma cell lines as well as in cells from the blood and marrow of patients with these malignancies. Hypermethylation of latexin promoter in tumor cells was revealed by researchers. Latexin caused growth inhibition of lymphoma cells by significantly increasing apoptosis through the down-regulation of anti-apoptotic genes Bcl-2 and Pim-2. These results are consistent with a tumor suppressor role for latexin and suggest that latexin may have clinical efficacy in the treatment of malignancies.