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Objective:To study the effects of activating protein kinase C (PKC)on oral squamous-cell cancer(OSCC) cell epithelial-mesenchymal transition(EMT).Methods:Plasmid pCMV6-AC-GFP-P120ctn was used to transfect HN12 cells to make P120-catenin (120ctn) overexpress and thereafter PKC activator PMA (phorbol 12-myristate 13-acetate) was added to the culture.Real-time fluorescent quantitative PCR and Western blot were adopted to test mRNA and protein expression of PKC,P120ctn,E-cadherin(E-cad),N-cadherin(N-cad) and Vimentin(Vim).Transwell cell invasion and cell migration assay were used to test the invasion and migration capacity before and after the activation.Results:When PKC was activated by PMA,the expression of P120ctn and E-cad were decreased,the cell morphology changed,nRNA and protein expression of mesenchymal marker protein N-cad and Vim increased significantly.Meanwhile,the migration and invasion capacity of the tumor cells increased significantly(P ＜ 0.05).Conclusion:In OSCC cells,PKC may be involved in promoting EMT and the metastasis and invasion by adjusting P120ctn/E-cad expression and cell adhesion.
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AIM: Oral squamous cell carcinoma (OSCC) is the eighth most common cause of cancer death. OSCC cells can easily invade tissues and metastasize to the cervical lymph nodes. Understanding the molecular basis of OSCC metastasis would facilitate the development of new therapeutic approaches to the disease. MATERIALS AND METHODS: To identify the potential role of catenin (P120ctn) in the progression of OSCC, HN4 cells (derived from a primary OSCC) and HN12 cells (derived from a lymph node metastasis in the same patient) were used in the present study. The samples of 28 patients with OSCC were examined to determine the expression of P120ctn and E‑cadherin (E‑cad; E: Epithelial) in vivo. Then, P120ctn was subsequently knocked down in HN4 cells (HN4/shP120ctn) and overexpressed in HN12 cells (HN12/P120ctn). Invasion and migration capacity, as well as the expression of the epithelial‑to‑mesenchymal transition (EMT) markers N‑cadherin and vimentin were detected. RESULTS: The results showed a positive correlation between the expression of P120ctn and E‑cad in OSCC samples. The overexpression of P120ctn led to a decrease in both invasion and migration capacity of HN12 cells accompanied by a decrease in EMT markers. In contrast, knockdown of P120ctn led to an increase in both invasion and migration capacity accompanied by an increase in EMT markers. CONCLUSION: Considered together, we concluded that P120ctn might regulate EMT in OSCC through E‑cad. The proper expression of P120ctn might therefore serve as a therapeutic goal for the inhibition of OSCC progression.
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Objective To investigate the regulating function of p120-catenin (p120ctn) on proliferation and invasion of human bladder cancer cell T24.Methods Special siRNA was used to silence the expression of p120ctn in T24 cells.MTT assay was used to examine the T24 cell growth rate.The invasion of T24 cells and the control cells were measured by transwell chamber assay.Results The silencing of p120ctn could improve the proliferation and the invasiveness of T24 tumor cells.Transwell chamber assay showed that the in vitro invasion function of T24 cells was significant increase after p120ctn-siRNA.Conclusion p120ctn inhibited the bladder cancer proliferation and invasiveness of bladder carcinoma cells.
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Objective:To study the expression of E-cadherin and P120ctn in nasopharyngeal carcinoma tissues, and to investigate their relationship and the relation with clinico-pathological features. Methods Two-step immuno-histochemical staining was applied to detect the expression of E-cadherin and P120ctn in formalin fixation and paraffin-embedded specimens from 56 cases with nasopharyngeal carcinoma and 15 cases with normal nasopharyngeal epithelia. Result:The abnormal expression rates of E-cadherin and P120ctn in the 56 cases of NPC tissues were 64.29% and 67.86% respectively, mainly with reduction of expression membrane and with the expression of cytoplasm; 6.67% of the 15 comparative normal cases of nasopharyngitis had abnormal expression of E-cadherin and P120ctn The differences were statistically significant. The abnormal expression rates of E-cadherin and P120ctn in NPC tissues were 71.43% and 85.71% respectively in low differentiated cancer group, which was obviously higher than the rates-42.86% and 36.29%-in high and middle differentiated cancer group. The 80.00% and 85.00% abnormal expression rate in the group with cervical lymph node metastases was higher than that in the group without cervical lymph node metastases(52.78%, 58.33%). The abnormal expression rate of E-cadherin and P120ctn(76. 92%,84.62%) in the third and forth phases was higher than that in the first and second phases (46.66%, 53. 33%). The differences were statistically significant (P<0.05). There were all together 12 co-expression cases of P120ctn and E-cadherin and 28 abnormal co-expression cases in the 56 cases of NPC tissues, which was of obvious consistency and correlation, with the relevant indexes: rs=0.5217 and P<0.01. Conclusion: The abnormal expression of E-cadherin and P120ctn is closely related to the degree of differentiation, clinical stage and cervical lymph node metastasis, and they join in the process of NPC initiation, progression, invasion and metastasis.
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To investigate p120 catenin Mrna expression in Non-Hodgkin's lymphoma (NHL) cell lines (U937, Raji, Jurkat and Molt4) and normal lymphocytes and explore the relationship between p120 catenin and Non-Hodgkin's lymphoma, total RNA sample was extracted by using TRIzol and reversely transcripted into Cdna. Polymerase chain reaction was performed to detect Mrna expression of p120 catenin in NHL cell lines U937, Raji, Jurkat and Molt4. Normal lymphocytes were used as control. It was found expressions of p120 catenin 1A and 3A Mrna were high in above-mentioned NHL cell lines, but neither p120 catenin 1A nor 3A was found in normal lymphocytes as shown by RT-PCR. It is concluded that both P120ctn1A and P120ctn3A Mrna transcripts were found in all NHL cell lines U937, Raji, Jurkat and Molt4 but they don't exist in normal lymphocytes, suggesting p120ctn possibly is of importance in diagnosis and therapy of lymphoma.