Abstract
BackgroundThe cellular apoptosis susceptibility (CAS) protein is regarded as a proliferation-associated protein that associates with tumour proliferation as it associates with microtubule and functions in the mitotic spindle checkpoint. However, there is no any actual experimental study showing CAS (or CSE1 and CSE1L) can increase the proliferation of cancer cells. Previous pathological study has reported that CAS was strongly positive stained in all of the metastasis melanoma that be examined. Thus, CAS may regulate the invasion and metastasis of cancers. CAS is highly expressed in cancers; if CAS is associated with cancer proliferation, then increased CAS expression should be able to increase the proliferation of cancer cells. We studied whether increased CAS expression can increase cancer cell proliferation and whether CAS regulates the invasion of cancer cells.MethodsWe enhanced or reduced CAS expression by transfecting CAS or anti-CAS expression vectors into human MCF-7 breast cancer cells. The proliferations of cells were determined by trypan blue exclusion assay and flow cytometry analysis. Invasion of cancer cells were determined by matrigel-based invasion assay.ResultsOur studies showed that increased CAS expression was unable to enhance cancer cell proliferation. Immunofluorescence showed CAS was distributed in cytoplasm areas near cell membrane and cell protrusions. CAS was localized in cytoplasmic vesicle and immunogold electronmicroscopy showed CAS was located in vesicle membrane. CAS overexpression enhanced matrix metalloproteinase-2 (MMP-2) secretion and cancer cell invasion. Animal experiments showed CAS reduction inhibited the metastasis of B16-F10 melanoma cells by 56% in C57BL/6 mice.ConclusionOur results indicate that CAS increases the invasion but not the proliferation of cancer cells. Thus, CAS plus ECM-degradation proteinases may be used as the markers for predicting the advance of tumour metastasis.
Highlights
The cellular apoptosis susceptibility (CAS) protein is regarded as a proliferationassociated protein that associates with tumour proliferation as it associates with microtubule and functions in the mitotic spindle checkpoint
CAS was identified in a study of an antisense DNA fragment that is capable of causing cell resistance to apoptosis induced by bacterial toxins and tumor necrosis factors [17]
CAS was identified in a study of an antisense DNA fragment that is capable of causing cell resistance to apoptosis induced by bacterial toxins [17]; reduction of cellular CAS levels by antisense DNA fragment against CAS is sufficient to obtain the cellular effect of CAS reduction
Summary
The cellular apoptosis susceptibility (CAS) protein is regarded as a proliferationassociated protein that associates with tumour proliferation as it associates with microtubule and functions in the mitotic spindle checkpoint. There is no any actual experimental study showing CAS (or CSE1 and CSE1L) can increase the proliferation of cancer cells. We studied whether increased CAS expression can increase cancer cell proliferation and whether CAS regulates the invasion of cancer cells. Many pathological studies demonstrated that the expression of CAS in tumors is related with tumor proliferation in cancer development [2,3,4,5]; there is no any actual experimental study showing CAS can increase cancer proliferation. Our recent study showed that increased CAS expression in human HT-29 colorectal cancer cells inhibited but not stimulated the proliferation of HT-29 cells [11]
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