Abstract
Cervical cancer is a leading cause of morbidity and mortality in women worldwide. Although the human papillomavirus (HPV) is considered the major causative agent of cervical cancer, yet the viral infection alone is not sufficient for cancer progression. The etiopathogenesis of cervical cancer is indeed complex; a precise understanding of the complex cellular/molecular mechanisms underlying the initiation, progression and/ or prevention of the uterine cervix is therefore essential. Autophagy is emerging as an important biological mechanism in targeting human cancers, including cervical cancer. Furthermore, autophagy, a process of cytoplasm and cellular organelle degradation in lysosomes, has been implicated in homeostasis. Autophagic flux may vary depending on the cell/tissue type, thereby altering cell fate under stress conditions leading to cell survival and/or cell death. Autophagy may in turn govern tumor metastasis and subsequent carcinogenesis. Inflammation is a known hallmark of cancer. Vascular insufficiency in tumors, including cervical tissue, leads to depletion of glucose and/or oxygen perturbing the osmotic milieu causing extracellular acidosis in the tumor microenvironment that may eventually result in autophagy. Thus, targeted manipulation of complex autophagic signaling may prove to be an innovative strategy in identification of clinically relevant biomarkers in cervical cancer in the near future.
Highlights
Cervical cancer has emerged as a leading cause of morbidity and mortality in women worldwide (Walboomers et al, 1999; Pandey et al, 2012)
Class III PI3K is the homologue of Beclin-1, and their bond through common helix domain directly results in the occurrence of autophagy; in this regulatory frame, Beclin-1 undertakes a central place because of its necessary function in the formation of autophagic vacuoles (Chen and Klionsky, 2011); several mammalian homologues of yeast autophagy-related genes (Atgs) have been identified, and the mechanisms of yeast autophagy are largely conserved in mammals
Autophagy flux/activity in the cell under GDconditions may be determined by western blot, wherein the conversion of the two known isoforms of LC-3A/B, I and II, may be monitored on SDS-PAGE; a representative data showing the light chain 3 (LC3) isoforms (LC3 Antibody was purchased/ procured from Cell Signaling Technology Inc., USA) during a time-course (0-48 h.) experiment carried out in colorectal carcinoma cell line SW-480 (GAPDH was used an an internal reference) has been depicted in **Figure 1b
Summary
Cervical cancer has emerged as a leading cause of morbidity and mortality in women worldwide (Walboomers et al, 1999; Pandey et al, 2012). A process of cytoplasm and cellular organelle degradation in lysosomes, has been implicated in homeostasis and under altered biological/metabolic conditions such as cellular stress, the cell may undergo survival and/or cell death; autophagy may in turn govern tumor metastasis and subsequent carcinogenesis (Janku et al, 2011; Kung et al, 2011; Mathew and White, 2011; Wu, 2012). One of the nonapoptotic cell death mechanisms, is characterized by engulfment of cytoplasm and organelles into double-membrane bound structures, autophagosomes, and delivery to and subsequent degradation in lysosomes; it may be triggered under physiological conditions, such as nutrient starvation or in response to various stress stimuli, such as radiations or cytotoxic compounds (Yang and Klionsky, 2003; Liu et al, 2011). Research in the past decade has substantially increased our understanding of non-apoptotic programmed cell death events, such as lysosomal-mediated cell death, necroptosis and autophagy (Kreuzaler and Watson, 2012) cross-talk between various components of each of these cell death pathways further governs subsequent cancer progression under stressful conditions
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
