Search

Objective: This study aimed to investigate the expressions and significance of KAI1/CD82 and cyclin D1 in laryngeal squamous cell carcinoma (LSCC)., Methods: Real-time quantitative PCR (Q-PCR) and Western blot assay were employed to detect the expressions of KAI1/CD82 and cyclin D1 in the laryngeal tissues of 86 LSCC patients, 32 patients with laryngeal polyp and 38 patients with laryngeal leukoplakia, and the influence of both proteins on the clinicopathological features and survival of LSCC patients., Results: The changes in mRNA and protein expressions of KAI1/CD82 and cyclin D1 were consistent in three groups, and the expressions of KAI1/CD82 and cyclin D1 were significantly different among three groups (P<0.01 or <0.05). The KAI1/CD82 expression in patients with TNM stage III-IV LSCC, poorly differentiated LSCC, clinical stage III-IV LSCC or lymph node metastasis was markedly lower than that in those with TNM stage I-II LSCC, well differentiated LSCC, clinical stage I-II LSCC or no lymph node metastasis (P<0.01 or <0.05). However, there was no marked difference in KAI1/CD82 expression between males and females and among patients in different age groups (P>0.05). In LSCC patients positive for KAI1/CD82 protein expression, the median survival time was 76 months, which was significantly longer than that in LSCC patients negative for KAI1/CD82 protein expression (48 months; X(2)=16.293, P=0.000). The Cyclin D1 expression in patients with TNM stage III-IV LSCC, poorly differentiated LSCC, or clinical stage III-IV LSCC was dramatically higher than that in patients with TNM stage I-II LSCC, well differentiated LSCC, or clinical stage I-II LSCC (P<0.01 or <0.05). However, no marked difference was noted in cyclin D1 expression between males and females, among patients in different age groups and between patients with and without lymph node metastasis (P>0.05). In LSCC patients positive for cyclin D1 protein expression, the median survival time was 40 months, which was markedly shorter than that in LSCC patients negative for cyclin D1 protein expression (X(2)=9.517, P=0.02). In LSCC patients, there was a negative correlation between KAI1/CD82 expression and cyclin D1 expression (X(2)=7.86, P<0.01)., Conclusion: KAI1/CD82 affects cell cycle. Both KAI1/CD82 and cyclin D1 are involved in the occurrence and development of LSCC, and may provide clinical information for evaluation of invasiveness, metastasis and prognosis of LSCC. Thus, KAI1/CD82 and cyclin D1 may serve as markers for determination of invasiveness, metastasis and prognosis of LSCC.

Objective: To study the effect of anti-tumor peptide of tumstatin on tumor growth of human laryngeal squamous carcinoma in nude mice and the underlying mechanism., Method: Nude mice model bearing laryngocarcinoma were established by using human laryngeal squamous carcinoma cell line (Hep-II). The animals were given tumstatin or PBS for 10 consecutive days. The volumes of the subcutaneous tumor were observed. The microstructure in which the general 2-step immunohistochemical examination was adopted and ultra-micro-structural changes of carcinoma after administration of tumstatin were observed under light and electron microscopes for pathology examination., Result: The differences was statistically significant in the net mice weight, tumor weight, tumor volume and tumor weight/net mice weight between the treatment group and the control group (P<0.01). The restrained percentage of tumor was 51.58%. The necrosis and apoptosis of the tumor cells and the angiogenesis reduction were found under light and electron microscope in the treatment group. MVD of the treatment group was lower than that of the control group (P<0.01)., Conclusion: Tumstatin can significantly restrain the development of laryngocarcinoma.

MicroRNAs (miRNA) are a class of small noncoding RNAs that regulate the expression of their target genes. The aim of the present study was to explore the effects of miR-206 on laryngeal suamous cell carcinoma (LSCC) cells. The expression level of miR-206 was quantified by qRT-PCR in primary LSCC tissues and corresponding adjacent non-neoplastic tissues. MTT, Matrigel invasion assays and flow cytometry methods were used to test the proliferation, invasion and apoptosis of MiR-206 transfection LSCC cells and a mouse model was used to investigate tumorigenesis. MiR-206 was significantly down regulated in the LSCC tissues. Inverse correlation of miR-206 expression was found with the T grade, nodal metastasis and clinical stage of LSCC. Cell proliferation, migration, invasion and tumorigenesis in the LSCC cells were significantly inhibited and apoptotic cells were also increased after miR-206 tansfection. Furthermore, miR-206 transfection down-regulated the expression of vascular endothelial growth factor (VEGF) in the LSCC cells. The loss of miR-206 may play an important role in the progress of LSCC and miR-206 may function as a novel tumor suppressed miRNA.

Objective: To study the apoptosis inducing effect of tumor necrosis factor related apoptosis-ligand (TRAIL) on human laryngeal squamous carcinoma Hep-2 cells and its effect mechanism., Method: The human laryngeal squamous carcinoma Hep-2 cell line was treated with different concentration of TRAIL in vitro. The inhibition ratio of tumor cells was determined by MTT colorimetric assay, the incidence of cell apoptosis was determined by flow cytometry method. The morphologic changes of laryngeal squamous carcinoma Hep-2 cell were observed with transmission electron microscope., Result: In vitro, all the different concentrations of TRAIL inhibited laryngeal squamous carcinoma cell's growth. The inhibited growth ratio showed significant concentration-dependence. The concentrations for inducing apoptosis-ratio(TRAIL 1, 10, 100 microg/L) determined by flow cytometry was (11.49 +/- 0.36)%, (22.31 +/- 0. 82)%, (59.64 +/- 1.10)% respectively in the study group, and (3.13 +/- 0.12)% in the control group, which was significantly different between these two groups (P < 0. 01)., Conclusion: In vitro, TRAIL inhibited the growth of human laryngeal squamous carcinoma Hep-2 cells. The induced apoptosis of TRAIL shows significant concentration- independence. TRAIL inhibits the growth of human laryngeal squamous carcinoma Hep-2 cells trough inducing apoptosis.

Objective: To investigate the inhibitive role of lentivirus mediated MMP-9 gene silence in the growth of laryngeal cancer xenografts., Method: The nude mouse model of laryngeal squamous carcinoma was established and RNA interference (RNAi) technic was used. Recombinant MMP-9-RNAi-Lentivirus was intratumoral injected while the empty vector lentivirus was taken as control. After the treatment, tumor inhibitive effect was observed and western-blot was used to test the expression of MMP-9 in the xenografts. Finally, the PCNA expression in xenografts were examined with immunohistochemistry to evaluate proliferation change of the Hep-2 cells., Result: The average tumor weight was (1.484 +/- 0.391) g in group treated with MMP-9-RNAi-Lentivirus which was significantly lower than that (2.618 +/- 0.465) g in the control group (P < 0.05). The average tumor volume was (1.177 +/- 0.270) cm3 in group treated with MMP-9-RNAi-Lentivirus which was significantly lower than that (2.034 +/- 0.366) cm3 in the control group (P < 0.05) and the tumor inhibitive rate was 43.32%. Western-blot showed there were 7 cases of xenografts with MMP-9 protein negative expression and the other 3 cases were tested with weak positive expression in the treated group xenografts. Whereas all the 10 cases of xenografts were tested with MMP-9 positive expression in the control group. Immunohistochemistry showed PCNA index in treated group was (55.41 +/- 8.77)% which was obviously lower than that (77.04 +/- 6.91)% in control group (P < 0.01)., Conclusion: The growth and proliferation of laryngeal cancer could be inhibited by recombinant MMP-9-RNAi-Lentivirus.