Cellular Signaling Mechanisms in Pancreatic Apoptosis

Ali, Nawab; MacLeod, Stewart L.; Hine, R. Jean; Chowdhury, Parimal

doi:10.1007/978-1-4020-9597-9_13

Cited by 3 publications

References 168 publications

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Changes in cellular levels of inositol polyphosphates during apoptosis

2010

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Accumulations of higher inositol polyphosphates, diphosphoinositol polyphosphates or pyrophosphates, have been implicated to mediate cellular apoptosis. Whether cellular levels of lower inositol phosphates (lower than inositol hexakisphosphates) change during apoptosis is not known, although these inositol phosphates are known to play crucial roles in a number of cellular signaling processes including calcium mobilization. Therefore, in this study, we have examined changes in cellular levels of inositol phosphates following metabolic labeling of these compounds by [(3)H]myo-inositol and induction of apoptosis. The levels of inositol mono- and bis-phosphates were increased, whereas the levels of inositol tris- and tetrakis-phosphates decreased significantly with an increasing rate of apoptosis induced by etoposide in a dose-dependent manner. NaF treatment, which increased the rate of apoptosis in a time- and dose-dependent manner, also increased the levels of inositol mono- and bis-phosphates and drastically reduced the levels of inositol tris- and tetrakis-phosphates. Prior treatment with antimycin A, a strategy used to reverse the NaF-induced accumulations of higher InsPs, partially reduced the effects of NaF on apoptosis as well as the levels of lower InsPs. Taken together, our results suggest that cellular levels of lower InsPs are altered during apoptosis.

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Changes in cellular levels of inositol polyphosphates during apoptosis

2010

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Inositol Hexakisphosphate Mediates Apoptosis in Human Breast Adenocarcinoma McF-7 Cell Line via Intrinsic Pathway

Agarwal¹,

Ali²,

Tarasenko³

2010

AIP Conference Proceedings

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Molecular signaling mechanisms of apoptosis in hereditary non-polyposis colorectal cancer

Hassen

Ali²,

Chowdhury³

2012

WJGP

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Colorectal cancer is the second most leading cause of cancer related deaths in the western countries. One of the forms of colorectal cancer is hereditary nonpolyposis colorectal cancer (HNPCC), also known as "Lynch syndrome". It is the most common hereditary form of cancer accounting for 5%-10% of all colon cancers. HNPCC is a dominant autosomal genetic disorder caused by germ line mutations in mismatch repair genes. Human mismatch repair genes play a crucial role in genetic stability of DNA, the inactivation of which results in an increased rate of mutation and often a loss of mismatch repair function. Recent studies have shown that certain mismatch repair genes are involved in the regulation of key cellular processes including apoptosis. Thus, differential expression of mismatch repair genes particularly the contributions of MLH1 and MSH2 play important roles in therapeutic resistance to certain cytotoxic drugs such as cisplatin that is used normally as chemoprevention. An understanding of the role of mismatch repair genes in molecular signaling mechanism of apoptosis and its involvement in HNPCC needs attention for further work into this important area of cancer research, and this review article is intended to accomplish that goal of linkage of apoptosis with HNPCC. The current review was not intended to provide a comprehensive enumeration of the entire body of literature in the area of HNPCC or mismatch repair system or apoptosis; it is rather intended to focus primarily on the current state of knowledge of the role of mismatch repair proteins in molecular signaling mechanism of apoptosis as it relates to understanding of HNPCC.

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Cellular Signaling Mechanisms in Pancreatic Apoptosis

Cited by 3 publications

References 168 publications

Changes in cellular levels of inositol polyphosphates during apoptosis

Changes in cellular levels of inositol polyphosphates during apoptosis

Inositol Hexakisphosphate Mediates Apoptosis in Human Breast Adenocarcinoma McF-7 Cell Line via Intrinsic Pathway

Molecular signaling mechanisms of apoptosis in hereditary non-polyposis colorectal cancer

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