Caspase complex in laryngeal squamous cell carcinoma.

Caspases (cysteine-aspartic proteases) represent a family of enzymes that modify several functions crucial for cell homeostasis such as inflammation and apoptosis. According to their implication in the apoptotic pathways, caspases are characterized as initiators and executioners, respectively. In the first group have been inserted caspase-2,-8,-9, and -10, whereas caspase-3,-6, and-7 belong to the second category. All of these normal actions of the caspase complex that induce apoptosis are altered in carcinoma progression and establishment. In cancer tissues, programmed cell death is inhibited due to a deregulation in expression of apo- and anti-apoptotic proteins. This genetic imbalance drives the cancer cell to immortalization which reflects the aberrant tissue proliferation. For this reason, caspases and the other apoptotic molecules are considered as important targets for specific targeted therapeutic strategies for enhancing the apoptotic levels inside the malignant tumor cells cores. In the current review we explored the role of caspases deregulation in laryngeal squamous cell carcinoma (LSCC). In malignancies -including LSCC- its deregulation leads the cells to immortalization due to apoptosis inhibition and telomerase overexpression. Caspase-dependent apoptotic rates are decreased in LSCC. For this reason, caspases are considered a very promising target for applying targeted therapeutic strategies in order to enhance apoptosis in the corresponding patients suffering of LSCC.

Chromosomal instability in oral squamous cell carcinoma.

Oral squamous cell carcinoma (OSCC) demonstrates an increasing rate due to high risk Human Papilloma Virus (HR-HPV) persistent infection, and also to chronic cigarette and alcohol consumption. Gross chromosomal alterations (polysomy, aneuploidy, intra-chromosome rearrangements) and specific gene aberrations such as amplifications, deletions, point mutations combined or not with epigenetic ones (promoter methylations and miRNA deregulations) are responsible for the progressive transformation of normal squamous cell epithelia to the corresponding malignant. Chromosomal instability (CI) -based on structural or numerical abnormalities- leads to specific abnormal karyotypes combined or not with functional suppressor gene inactivation and oncogene overactivation in solid malignancies, including OSCC. Extensive cytogenetic analyses have shown that gross alterations (gains/losses) in chromosomes 3, 4, 7, 8, 9, 11, 14, 17, 18, 19 and also 20 form different CI patterns in OSCC, which in conjunction with an aggressive phenotype (presence of lymph nodal metastasis) negatively affect the prognosis in the corresponding patients. In the majority of OSCC cases, loss of chromosomal bands are almost equally detected compared with gains regarding the chromosomes referred above. In the current special molecular paper we explored the role of CI in the progression and biological behavior of OSCCs.