Abstract:Protein kinase B (Akt) plays a very significant role in various cancers including oral cancer. However, it has three isoforms (Akt1, Akt2, and Akt3) and they perform distinct functions and even play contrasting roles in different cancers. Therefore, it becomes essential to evaluate the isoform-specific role of Akt in oral cancer. In the present study, an attempt has been made to elucidate the isoform-specific role of Akt in oral cancer. The immunohistochemical analysis of oral cancer tissues showed an overexpr… Show more
“…In accordance with previous investigations including some in vivo and in vitro experiments [24] , [27] , [26] , [28] , [29] , [30] , [31] , [32] , [33] , [34] , [35] , [36] , [37] , [38] , [39] , [40] , [41] , [42] , [43] , [44] , [45] , [25] , [46] , [47] , [48] , [49] , [50] , [51] , [52] , [53] , [54] , [55] , [56] , [57] , [58] , [59] , [60] , [61] , [62] , [63] , [64] , [65] , the simulation results also suggest that abnormal over expressions of certain proteins and genes depicted in Table 3 play significant roles to maintain growth, proliferation and energy supply in mammalian cancer cells to survive. Under expressions of prolyl-hydroxylases (PHD) and tumor suppressing protein p53 are also important in this context.…”
Section: Introductionsupporting
confidence: 90%
“…12 (A) Immunohistochemical scores measured by Mao et al [56] has depicted that AKT expression is significantly higher in pancreatic cancer (91 cases) than that in normal pancreas (51 cases). Besides, Roy et al [57] has shown the deferentially expressed AKT isoforms in normal and malignant oral tissues through immunohistochemical analysis of the human samples, (B) Similar altered behavior of AKT has been shown by the computational results generated from the proposed model. Fig.…”
Section: Resultsmentioning
confidence: 53%
“…12 A). Besides, Roy et al [57] has shown the deferentially expressed AKT isoforms in normal and malignant oral tissues through immunohistochemical analysis of the human samples ( Fig. 12 A).…”
Section: Resultsmentioning
confidence: 98%
“…In support of our simulation results, we have found some previous investigations, including in vivo and in vitro experiments [28] , [29] , [30] , [31] , [32] , [33] , [34] , [35] , [36] , [37] , [38] , [39] , [40] , [41] , [42] , [43] , [44] , [64] , [65] , which show similar kinds of behavior. Besides, we have collected the recent in vivo / in vitro data [54] , [56] , [57] , [55] , [58] , [59] , [60] , [61] , [62] , [63] of human cancer cells to compare different mutations verified in experimental laboratories with our simulation results. Here, we have normalized the experimental data in .…”
“…In accordance with previous investigations including some in vivo and in vitro experiments [24] , [27] , [26] , [28] , [29] , [30] , [31] , [32] , [33] , [34] , [35] , [36] , [37] , [38] , [39] , [40] , [41] , [42] , [43] , [44] , [45] , [25] , [46] , [47] , [48] , [49] , [50] , [51] , [52] , [53] , [54] , [55] , [56] , [57] , [58] , [59] , [60] , [61] , [62] , [63] , [64] , [65] , the simulation results also suggest that abnormal over expressions of certain proteins and genes depicted in Table 3 play significant roles to maintain growth, proliferation and energy supply in mammalian cancer cells to survive. Under expressions of prolyl-hydroxylases (PHD) and tumor suppressing protein p53 are also important in this context.…”
Section: Introductionsupporting
confidence: 90%
“…12 (A) Immunohistochemical scores measured by Mao et al [56] has depicted that AKT expression is significantly higher in pancreatic cancer (91 cases) than that in normal pancreas (51 cases). Besides, Roy et al [57] has shown the deferentially expressed AKT isoforms in normal and malignant oral tissues through immunohistochemical analysis of the human samples, (B) Similar altered behavior of AKT has been shown by the computational results generated from the proposed model. Fig.…”
Section: Resultsmentioning
confidence: 53%
“…12 A). Besides, Roy et al [57] has shown the deferentially expressed AKT isoforms in normal and malignant oral tissues through immunohistochemical analysis of the human samples ( Fig. 12 A).…”
Section: Resultsmentioning
confidence: 98%
“…In support of our simulation results, we have found some previous investigations, including in vivo and in vitro experiments [28] , [29] , [30] , [31] , [32] , [33] , [34] , [35] , [36] , [37] , [38] , [39] , [40] , [41] , [42] , [43] , [44] , [64] , [65] , which show similar kinds of behavior. Besides, we have collected the recent in vivo / in vitro data [54] , [56] , [57] , [55] , [58] , [59] , [60] , [61] , [62] , [63] of human cancer cells to compare different mutations verified in experimental laboratories with our simulation results. Here, we have normalized the experimental data in .…”
“…Mounting evidence imply that the PI3K/Akt/mTOR pathway plays a crucial role in oncogenesis and is often reported to be activated in lung cancer [5,6,[50][51][52][53][54]. Aberrations in various messenger molecules of this pathway result in cancer cell proliferation, apoptosis inhibition, angiogenesis, and metastasis [55].…”
Section: Knockout Of Tipe2 Modulated Akt/mtor/nf-κb Signaling Axismentioning
Lung cancer represents the most common cause of cancer deaths in the world, constituting around 11.6% of all new cancer cases and 18.4% of cancer-related deaths. The propensity for early spread, lack of suitable biomarkers for early diagnosis, as well as prognosis and ineffective existing therapies, contribute to the poor survival rate of lung cancer. Therefore, there is an urgent need to develop novel biomarkers for early diagnosis and prognosis which in turn can facilitate newer therapeutic avenues for the management of this aggressive neoplasm. TIPE2 (tumor necrosis factor-α-induced protein 8-like 2), a recently identified cytoplasmic protein, possesses enormous potential in this regard. Immunohistochemical analysis showed that TIPE2 was significantly upregulated in different stages and grades of lung cancer tissues compared to normal lung tissues, implying its involvement in the positive regulation of lung cancer. Further, knockout of TIPE2 resulted in significantly reduced proliferation, survival, and migration of human lung cancer cells through modulation of the Akt/mTOR/NF-κB signaling axis. In addition, knockout of TIPE2 also caused arrest in the S phase of the cell cycle of lung cancer cells. As tobacco is the most predominant risk factor for lung cancer, we therefore evaluated the effect of TIPE2 in tobacco-mediated lung carcinogenesis as well. Our results showed that TIPE2 was involved in nicotine-, nicotine-derived nitrosamine ketone (NNK)-, N-nitrosonornicotine (NNN)-, and benzo[a]pyrene (BaP)-mediated lung cancer through inhibited proliferation, survival, and migration via modulation of nuclear factor kappa B (NF-κB)- and NF-κB-regulated gene products, which are involved in the regulation of diverse processes in lung cancer cells. Taken together, TIPE2 possesses an important role in the development and progression of lung cancer, particularly in tobacco-promoted lung cancer, and hence, specific targeting of it holds an enormous prospect in newer therapeutic interventions in lung cancer. However, these findings need to be validated in the in vivo and clinical settings to fully establish the diagnostic and prognostic importance of TIPE2 against lung cancer.
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