Role of CDC25 Protein and Research Paper

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Some evidence indicates tobacco and alcohol use as predisposing factors for ESCC (Shou et al., 2008, p. 19), but further studies are needed to explore this important question.

A final notable feature of the results is that they indicate widespread agreement on the implication of CDC25 protein and mRNA expression levels and subcellular localization in ESCC. Few studies of CDC25 enzymatic function/dysfunction appeared in the search results.

The results of the literature search highlight the importance of the problem of ESCC for two main reasons. First, the results suggest that a substantial amount of research has been done into this major clinical problem, the fourth leading cause of cancer deaths in China and a highly lethal form of carcinoma (Dong et al., 2010, p. 82). Second, the results suggest that ESCC could be a good system for studying the molecular basis of cell cycle progression. This is because ESCC involves dysfunction or dysregulation of CDC25, a key molecule involved in regulating the cell cycle in normal cells.

Conclusion

Based on the search results, there is a plethora of evidence implicating CDC25 overexpression in ESCC cells (as opposed to normal cells) as indicative of carcinoma, and as playing a causal role in the proliferation of cancer cells and cancer progression (Nishioka et al., 2001, p. 412) (Dong et al.

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, 2010, p. 81) (Shou et al., 2008, p. 1424) (Liu et al., 2008, p. 440). There is also evidence suggesting that a nuclear localization of CDC25 suggests poor prognosis in squamous cell carcinoma (Wang et al., 2010, p. 239).

There is less evidence that CDC25 biochemical dysfunction plays a role in ESCC. Biochemical studies of enzyme kinetics are lacking, and this additional information would help advance the field. For example, a study comparing enzymatic activity of CDC25 in cancer cells compared to normal cells would provide information about whether enzyme dysfunction, rather than just expression levels, is important for tumorigenesis and cancer progression.

The evidence is mounting that CDC25 expression level is important for causing (rather than just being correlated with) ESCC. However, studies are needed in which CDC25 level or enzymatic activity is inhibited in order to more definitively show a causal role for cell proliferation/cancer progression. If reducing CDC25 functional levels by antibody inhibition, chemical small molecule inhibition, or siRNA techniques blocks cell proliferation or cancer progression, this would be stronger evidence of a causal role for CDC25. Such a result would also open doors to possible therapeutic applications of inhibiting CDC25......

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