Rui Hai1, Qian You2, Fei Wu2, Guochun Qiu1, Qian Yang3, Liang Shu2, Linjun Xie2, Xiangyu Zhou4. 1. Department of Breast, Thyroid and Vessel Surgery, The Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Luzhou, China. 2. Department of General Surgery (Thyroid Surgery), The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China. 3. Department of Oncology, The Leshan People's Hospital, Leshan, 614000, China. 4. Department of General Surgery (Thyroid Surgery), The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China. xiangyuzhou971@vip.126.com.
Abstract
BACKGROUND: Semaphorin 3D (SEMA3D) plays an important role in the occurrence and development of multifarious cancers. However, the relationship between SEMA3D and papillary thyroid carcinoma (PTC) remains unclear. This study aimed to investigate the functions and mechanism of SEMA3D in papillary thyroid carcinoma (PTC). METHODS: The expression of SEMA3D in PTC tissues and cell lines was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Western blotting and immunohistochemistry (IHC) were used to detect the expression of the related proteins. CCK-8 and colony formation assays and Transwell assays were used to evaluate cell proliferation and migration, respectively. A xenograft model was induced to further verify the effect of SEMA3D in vivo. RESULTS: In this study, we found that SEMA3D was downregulated in PTC tissues and PTC cell lines (TPC-1 and BCPAP). The expression level of SEMA3D was significantly related to age (P < 0.01), extrathyroidal extension (P < 0.01), TNM stage (P < 0.01) and lymph node metastasis (P < 0.01). In vitro experiments showed that overexpression of SEMA3D inhibited the proliferation and migration of TPC-1 and BCPAP cells and that upregulated SEMA3D inhibited the phosphorylation of ERK and the expression of the phenotype-related proteins PCNA and MMP2. In addition, SEMA3D overexpression inhibited tumour growth in vivo. CONCLUSION: In this study, we found that SEMA3D is significantly downregulated in PTC tissues. SEMA3D inhibits the proliferation and migration of PTC cells and suppresses tumour growth in vivo, possibly partially through the MAPK/ERK signalling pathway, suggesting that SEMA3D may be a reliable molecular marker for the diagnosis and treatment of PTC.
BACKGROUND: Semaphorin 3D (SEMA3D) plays an important role in the occurrence and development of multifarious cancers. However, the relationship between SEMA3D and papillary thyroid carcinoma (PTC) remains unclear. This study aimed to investigate the functions and mechanism of SEMA3D in papillary thyroid carcinoma (PTC). METHODS: The expression of SEMA3D in PTC tissues and cell lines was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Western blotting and immunohistochemistry (IHC) were used to detect the expression of the related proteins. CCK-8 and colony formation assays and Transwell assays were used to evaluate cell proliferation and migration, respectively. A xenograft model was induced to further verify the effect of SEMA3D in vivo. RESULTS: In this study, we found that SEMA3D was downregulated in PTC tissues and PTC cell lines (TPC-1 and BCPAP). The expression level of SEMA3D was significantly related to age (P < 0.01), extrathyroidal extension (P < 0.01), TNM stage (P < 0.01) and lymph node metastasis (P < 0.01). In vitro experiments showed that overexpression of SEMA3D inhibited the proliferation and migration of TPC-1 and BCPAP cells and that upregulated SEMA3D inhibited the phosphorylation of ERK and the expression of the phenotype-related proteins PCNA and MMP2. In addition, SEMA3D overexpression inhibited tumour growth in vivo. CONCLUSION: In this study, we found that SEMA3D is significantly downregulated in PTC tissues. SEMA3D inhibits the proliferation and migration of PTC cells and suppresses tumour growth in vivo, possibly partially through the MAPK/ERK signalling pathway, suggesting that SEMA3D may be a reliable molecular marker for the diagnosis and treatment of PTC.