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Normally, with increasing mitosis, the telomere will shorten and eventually tiger apoptosis. However, many tumors and cancers, can activate the telomerase to lengthen the telomeres of the DNA strands, thereby rendering cells immortality. The way they do so is usually through interacting with hTERT (human Telomerase reverse transcriptase), which is a crucial catalytic subunit of telomerase complex. Numerous studies have found proteins that may act as regulators of hTERT [1-4]. NFX1 is one of them[5], increasing the expression of hTERT, therefore augmenting the telomerase activity. By interacting with NFX1, the HPV virus activates hTERT and turn normal cells to cancerous cells. Unfortunately, how many other partner proteins and the mechanisms of how HPV virus activate hTERT remains unclear. Here we improve on the previous conclusion that HPV virus is highly associated with NFX1-123 protein by taking a further step to see other potential proteins that may be involved in the process. Our results, over two hundred differential proteins, provide perspective research direction on the protein pathways.
Nearly 100,000 Indian women die of cervical cancer each year and many earn less than $360 annually [6], while according to the CDC, the 3 doses needed for complete vaccination cost almost $500. It's true that powerful HPV vaccine have been developed and approved, it's hardly available to people who need it the most. In china, people wait for months to be vaccinated, and the majority report immense difficulties in making appointments. Although there are several institutions that are trying hard to provide low-cost vaccines to developing countries, the number of vaccines is simply too small. Our results allow people with higher risk of HPV infection to be diagnosed, thus the distribution of vaccine can be more efficient. The diagnostic result will also help people in deciding whether the vaccine is necessary or urgent, thereby alleviating the vaccine shortage while maximizing its influence.
We improved on the accuracy of our results in two ways. First, by performing western bolt after SDS-Page, we clearly confirm the successful overexpression of NFX1 protein in our cells. More convincingly, we performed two Mass Spectra, using two different methods to prepare the sample and set up comparisons. Then we draw our conclusion based on the two results combined, which means that the differential proteins we identified are highly likely to be associated with NFX1 and HPV virus. Our conclusion is firm and validated, backed up with solid data.

[1]Regulation of telomerase activity by the p53 family member p73.
Beitzinger M, Oswald C, Beinoraviciute-Kellner R, Stiewe T
Oncogene. 2006 Feb 9; 25(6):813-26.

[2]C-terminal p73 isoforms repress transcriptional activity of the human telomerase reverse transcriptase (hTERT) promoter.
Racek T, Mise N, Li Z, Stoll A, Pützer BM
J Biol Chem. 2005 Dec 9; 280(49):40402-5.

[3]p53-dependent down-regulation of telomerase is mediated by p21waf1.
Shats I, Milyavsky M, Tang X, Stambolsky P, Erez N, Brosh R, Kogan I, Braunstein I, Tzukerman M, Ginsberg D, Rotter V
J Biol Chem. 2004 Dec 3; 279(49):50976-85.

[4]Function of AP-1 in transcription of the telomerase reverse transcriptase gene (TERT) in human and mouse cells.
Takakura M, Kyo S, Inoue M, Wright WE, Shay JW
Mol Cell Biol. 2005 Sep; 25(18):8037-43.

[5]NFX1-123 Increases hTERT Expression and Telomerase Activity Posttranscriptionally in Human Papillomavirus Type 16 E6 Keratinocytes
Rachel A. Katzenellenbogen, Portia Vliet-Gregg, Mei Xu, Denise A. Galloway
Journal of Virology Jun 2009, 83 (13) 6446-6456; DOI: 10.1128/JVI.02556-08

[6] Cervical cancer fact sheet. U.S. Department of Health and Human Services https://report.nih.gov/nihfactsheets/viewfactsheet.aspx?csid=76