Mors [19]. In breast cancer, expression of PKCa correlates with high histological grade and proliferation rate [17]. By contrast, one study reported that ovarian carcinoma exhibited decreasing in PKCa expression with increasing histological grade [29]. We found PKCa Cyproconazole site protein overexpression to be associated with histological grade and tumor differentiation in gastric carcinoma. In addition, we found that PKCa-positive high-grade dysplastic glands, precursor lesions of intestinal type carcinoma, were frequently 25033180 observed in intestinal type carcinomas with PKCa protein overexpression. The PKCa protein is thus thought to be involved in the early stage of gastric carcinogenesis. PKCa has been thought to play an important role in tumor progression. It has been Chebulagic acid chemical information implicated in several cancer-related processes, such as invasion and metastasis [10]. The role of PKCa in regulating tumor growth and development is clearly complex and highly tissue-dependent. In some cases PKCa acts as a tumor promoter, and in others it functions as a tumor suppressor [13]. In current immunohistochemical study, expression of PKCa protein was negatively statistically correlated to depth of invasion, angiolymphatic invasion, pathologic stage, and distant metastasis. We thus conduct that PKCa protein acts as a tumor suppressor, and downregulates gastric carcinoma progression. PKCa has been reported to be a prognostic marker in human cancers. In Kong’s study, high level PKCa predicted a shortened recurrence-free survival in patients with superficial bladder carcinomas [28]. Haughian et al demonstrated that PKCa level may be a prognostic indicator of aggressive endometrial cancers [19]. Patients with higher PKCa mRNA expression in hepatocellular carcinomas have a significantly decreased survival rate [21]. For patients with breast cancer, the prognostic significance of PKCa is controversial. L ne et al reported that patients with PKCa-positive breast carcinoma had a poorer survival rate [17], but Kerfoot et al found that PKCa was downregulated in advanced breast carcinoma [16]. Although no statistical significance via Kaplan-Meier method, our study showed a tendency for patients with PKCa protein overexpression to have a longer overall survival and disease free survival than those without overexpression. Furthermore, we found that PKCa protein overexpression was a significant independent prognostic factor for gastric carcinoma in multivariate analysis. Patients with PKCa protein overexpression had a statistically significant longer survival period. In our previous study, we demonstrated that PKCa mRNA expression was upregulated and associated with distant metastasis in gastric carcinoma, and that PKCa mRNA overexpression predicted poor outcome [15]. Considering the results of that study together with those of the current one, we concluded that in patients with advanced gastric carcinomas, PKCa mRNA plays a promoting role in decreased survival, whereas PKCa protein hasPKCa Protein Overexpression in Gastric Carcinomaan opposing effect to suppress cancer progression and decrease cancer mortality. Several hypotheses might account for this finding. First, PKCa protein is subjected to complete proteolysis during or preceding late-stage gastric cancers. A previous study has documented that the activation and degradation of PKC isoforms were controlled spatially and temporally [30]. Second, post-transcriptional processing and RNA splicing might be responsible for the opposite effect.Mors [19]. In breast cancer, expression of PKCa correlates with high histological grade and proliferation rate [17]. By contrast, one study reported that ovarian carcinoma exhibited decreasing in PKCa expression with increasing histological grade [29]. We found PKCa protein overexpression to be associated with histological grade and tumor differentiation in gastric carcinoma. In addition, we found that PKCa-positive high-grade dysplastic glands, precursor lesions of intestinal type carcinoma, were frequently 25033180 observed in intestinal type carcinomas with PKCa protein overexpression. The PKCa protein is thus thought to be involved in the early stage of gastric carcinogenesis. PKCa has been thought to play an important role in tumor progression. It has been implicated in several cancer-related processes, such as invasion and metastasis [10]. The role of PKCa in regulating tumor growth and development is clearly complex and highly tissue-dependent. In some cases PKCa acts as a tumor promoter, and in others it functions as a tumor suppressor [13]. In current immunohistochemical study, expression of PKCa protein was negatively statistically correlated to depth of invasion, angiolymphatic invasion, pathologic stage, and distant metastasis. We thus conduct that PKCa protein acts as a tumor suppressor, and downregulates gastric carcinoma progression. PKCa has been reported to be a prognostic marker in human cancers. In Kong’s study, high level PKCa predicted a shortened recurrence-free survival in patients with superficial bladder carcinomas [28]. Haughian et al demonstrated that PKCa level may be a prognostic indicator of aggressive endometrial cancers [19]. Patients with higher PKCa mRNA expression in hepatocellular carcinomas have a significantly decreased survival rate [21]. For patients with breast cancer, the prognostic significance of PKCa is controversial. L ne et al reported that patients with PKCa-positive breast carcinoma had a poorer survival rate [17], but Kerfoot et al found that PKCa was downregulated in advanced breast carcinoma [16]. Although no statistical significance via Kaplan-Meier method, our study showed a tendency for patients with PKCa protein overexpression to have a longer overall survival and disease free survival than those without overexpression. Furthermore, we found that PKCa protein overexpression was a significant independent prognostic factor for gastric carcinoma in multivariate analysis. Patients with PKCa protein overexpression had a statistically significant longer survival period. In our previous study, we demonstrated that PKCa mRNA expression was upregulated and associated with distant metastasis in gastric carcinoma, and that PKCa mRNA overexpression predicted poor outcome [15]. Considering the results of that study together with those of the current one, we concluded that in patients with advanced gastric carcinomas, PKCa mRNA plays a promoting role in decreased survival, whereas PKCa protein hasPKCa Protein Overexpression in Gastric Carcinomaan opposing effect to suppress cancer progression and decrease cancer mortality. Several hypotheses might account for this finding. First, PKCa protein is subjected to complete proteolysis during or preceding late-stage gastric cancers. A previous study has documented that the activation and degradation of PKC isoforms were controlled spatially and temporally [30]. Second, post-transcriptional processing and RNA splicing might be responsible for the opposite effect.
