Cervical cancer is a leading cause of morbidity and mortality in women worldwide. Although the humanpapillomavirus (HPV) is considered the major causative agent of cervical cancer, yet the viral infection aloneis not sufficient for cancer progression. The etiopathogenesis of cervical cancer is indeed complex; a preciseunderstanding 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 biologicalmechanism in targeting human cancers, including cervical cancer. Furthermore, autophagy, a process ofcytoplasm and cellular organelle degradation in lysosomes, has been implicated in homeostasis. Autophagicflux may vary depending on the cell/tissue type, thereby altering cell fate under stress conditions leading to cellsurvival 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, leadsto depletion of glucose and/or oxygen perturbing the osmotic mileu causing extracellular acidosis in the tumormicroenvironment that may eventually result in autophagy. Thus, targeted manipulation of complex autophagicsignaling may prove to be an innovative strategy in identification of clinically relevant biomarkers in cervicalcancer in the near future.
)