Sample A: Cover Page of Thesis, Project, or Dissertation Proposal

of cells, and abnormal cytokinesis can lead to spontaneous abortions, congenital malformations,
polyploidy and cancer predisposition [15, 19].
Similarly, EMP2 was significantly down regulated in the NSCLC samples. EMP2 has been
demonstrated to down-regulate caveolin-1 production [20], with up-regulated caveolin-1, CAV1,
inducing filopodia and facilitating metastasis in lung adenocarcinoma [21]. Caveolin-1 is
essential for the formation of caveoli formation, the plasma membrane invaginations which alter
the morphology of the plasma membrane [20]. The invaginations are essential for cholesterol
transport, localization of signal transduction, coordination with microtubules for membrane
trafficking, and regulation of NOS3, while oncogenic implications have been the subject of
conflicting reports for different cancer types [20, 22-24]. The caveolae structures constantly
recycle between the cell-to-cell contact points along the cell membrane, endosomes, and Golgi
network, while during mitosis they localize along the contractile ring [23, 25].
Additionally, the DNA-damaging ROS H2O2 is a mitotic signal messenger [26], which catalase
rapidly degrades [27]. Catalase (CAT) was demonstrated to accelerate the degradation of p53
proteins, thereby preventing ceramide induced apoptosis [27], while IGF-1 was demonstrated to
restore catalase activation through inhibition of PI-3-Akt inhibition at CAV1 localized
microdomains [28]. We observed significant upregulation of CAT in the normal samples.
Similarly, stratifin is induced by DNA-damage via p53 activation and regulates G2 cell cycle
arrest through positive feedback upon p53 [29, 30]. Conversely, it has been reported the stratifin
is activated by IGF1 in a manner independent of p53 activation [31]. Methylated sequesence of
stratifin has been reported in several cancers [30] and improper regulation may explain cancers
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