OBJECTIVE: This study aimed to investigate the expression and significance of ATF-3 in laryngeal squamous cell carcinoma (LSCC). METHODS: Expression of ATF-3 was examined using immunohistochemistry methods in samples from 83 cases of LSCC carcinoma. MTT assay was used to detect proliferation of Hep-2 cells after ATF-3 knocked down by siRNA lentivirus. A mouse model was used to investigate the inhibitive role of ATF-3 siRNA in LSCC xenografts. Realtime RCR was used to detect Cyclin D1 expression after ATF-3 downregulation in Hep-2 cells. RESULTS: The expression of ATF-3 was positively detected in all the 83 cases of LSCC cancer tissues while Only 4 cases of adjacent non-neoplastic tissues were detected with positive ATF-3 expression. The ATF-3 expression was statistically related with T stage, neck nodal metastasis, clinical stage and prognosis of LSCC. Both cell proliferation in vitro and tumor growth in vivo were suppressed after ATF-3 knockdown. Furthermore, the expression of Cyclin D1 was decreased after ATF-3 downregulation in Hep-2 cells. CONCLUSION: ATF-3 is involved in the progress of LSCC, and may provide clinical information for evaluation of prognosis of LSCC. The oncologic role of ATF-3 may be correlated with Cyclin D1 regulation.
OBJECTIVE: This study aimed to investigate the expression and significance of ATF-3 in laryngeal squamous cell carcinoma (LSCC). METHODS: Expression of ATF-3 was examined using immunohistochemistry methods in samples from 83 cases of LSCC carcinoma. MTT assay was used to detect proliferation of Hep-2 cells after ATF-3 knocked down by siRNA lentivirus. A mouse model was used to investigate the inhibitive role of ATF-3 siRNA in LSCC xenografts. Realtime RCR was used to detect Cyclin D1 expression after ATF-3 downregulation in Hep-2 cells. RESULTS: The expression of ATF-3 was positively detected in all the 83 cases of LSCC cancer tissues while Only 4 cases of adjacent non-neoplastic tissues were detected with positive ATF-3 expression. The ATF-3 expression was statistically related with T stage, neck nodal metastasis, clinical stage and prognosis of LSCC. Both cell proliferation in vitro and tumor growth in vivo were suppressed after ATF-3 knockdown. Furthermore, the expression of Cyclin D1 was decreased after ATF-3 downregulation in Hep-2 cells. CONCLUSION:ATF-3 is involved in the progress of LSCC, and may provide clinical information for evaluation of prognosis of LSCC. The oncologic role of ATF-3 may be correlated with Cyclin D1 regulation.
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