Kumar Dodda Venkatesh, Sivaranjani Y, Rao Guttikonda Venkateswara
Department of Oral Pathology and Microbiology, Mamata Dental College, Khammam, Telangana, India.
J Oral Maxillofac Pathol. 2020 Sep-Dec;24(3):580. doi: 10.4103/jomfp.JOMFP_244_19. Epub 2021 Jan 9.
The kallikrein (KLK) family of genes consists of 15 members, many of which are highly expressed in number of cancers compared to their normal parent tissues. KLK7 was initially characterized as an enzyme implicated in the degradation of intercellular cohesive structures in the stratum corneum of stratified squamous epithelia, preceding desquamation in the skin. It catalyzes the degradation of desmosomes in the outermost layer of skin and permits cell shedding to take place at the skin surface. Overexpression of KLK7 in tumor cells has been reported to significantly enhance the invasive potential in intracranial malignancies and ovarian cancer cells. Thus, KLK7 could contribute to the degradation of extracellular matrices in oral squamous cell carcinoma (OSCC) tissues, promoting invasion of neoplastic cells locally and facilitating metastasis to regional lymph nodes. The objectives of the present study were to compare the expression of KLK 7 in normal subjects and patients with OSCC, to correlate the expression of KLK 7 with respect to the clinical staging of OSCC and to evaluate the expression of KLK 7with respect to different histopathological grades of OSCC.
Thirty cases of OSCC were staged clinically and graded histopathologically. The immunohistochemical method was used to detect the expression of KLK 7 in OSCC. The scores obtained were documented and compared statistically.
KLK 7 immunoreactivity was noticed in all cases of OSCC. A statistically significant difference was observed in immunoreactivity of KLK 7 between the normal and OSCC ( = 0.0001*) and in different histopathological grades ( = 0.0001*) and in different clinical stages ( = 0.0127*) of OSCC using Kruskal-Wallis analysis of variance test.
The KLK 7 immunoexpression histopathologically increased from low grade to high grade and clinically from Stage 1 to Stage 4 in OSCC. Hence, increased expression of KLK 7 may be related to poor prognosis in patients with OSCC.
激肽释放酶（KLK）基因家族由15个成员组成，与正常组织相比，其中许多成员在多种癌症中高表达。KLK7最初被表征为一种参与分层鳞状上皮角质层细胞间黏附结构降解的酶，先于皮肤脱屑过程。它催化皮肤最外层桥粒的降解，使细胞能够在皮肤表面脱落。据报道，肿瘤细胞中KLK7的过表达可显著增强颅内恶性肿瘤和卵巢癌细胞的侵袭潜能。因此，KLK7可能参与口腔鳞状细胞癌（OSCC）组织细胞外基质的降解，促进肿瘤细胞的局部侵袭并便于转移至区域淋巴结。本研究的目的是比较KLK7在正常受试者和OSCC患者中的表达，将KLK7的表达与OSCC的临床分期相关联，并评估KLK7在不同组织病理学分级的OSCC中的表达。
30例OSCC患者进行了临床分期和组织病理学分级。采用免疫组织化学方法检测OSCC中KLK7的表达。记录所得分数并进行统计学比较。
所有OSCC病例均检测到KLK7免疫反应性。使用Kruskal-Wallis方差分析检验，观察到正常组织与OSCC之间（P = 0.0001*）、不同组织病理学分级之间（P = 0.0001*）以及OSCC不同临床分期之间（P = 0.0127*）KLK7免疫反应性存在统计学显著差异。
在OSCC中，KLK7免疫表达在组织病理学上从低级别到高级别增加，在临床上从1期到4期增加。因此，KLK7表达增加可能与OSCC患者的不良预后相关。
