The Third Peoples Hospital of Jinan City

Jinan, China

The Third Peoples Hospital of Jinan City

Jinan, China
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Yan J.,Shandong Academy of Sciences | Zhang Y.,The Third Peoples Hospital of Jinan City | Ren C.,The Third Peoples Hospital of Jinan City | Shi W.,The Third Peoples Hospital of Jinan City | Chen L.,Shandong Academy of Sciences
Tumor Biology | Year: 2015

Nuclear protein C23 and epidermal growth factor receptor (EGFR) are reported to be correlated with cervical cancer (CC). However the correlations between C23 and EGFR were rarely reported. Here, this study explored the effects of C23 in activation of EGFR signaling pathway. In our study, immunohistochemistry was used to identify the expression of C23 or EGFR in CC tissues. The level of the phosphorylated EGFR was observed by western blot, and cell invasion capacity was detected by Transwell assay. In this study, we found that C23 and EGFR were highly expressed in cervical cancer tissues, while C23 on the cell surface mainly expressed in CC tissues with lymph node metastasis, and was correlated to EGFR statistically. In vitro, western blot showed that either anti-C23 or anti-EGFR antibodies can inhibit the phosphorlation of EGFR with significant differences (p < 0.01). Besides, based on Transwell assay, the number of membrane-invading cells was reduced significantly in anti-C23 group, and no significant difference was found compared with anti-EGFR treatment (p > 0.05). In conclusion, C23 on the cell surface may be a kind of indispensable component in activation of EGFR signaling, by which C23 can participate in the growth and invasion of tumors. C23 antagonists may provide a new field for cervical cancer therapy. © 2015 International Society of Oncology and BioMarkers (ISOBM)


Yan J.,Shandong Academy of Sciences | Zhang Y.,The Third Peoples Hospital Of Jinan City | Shi W.,The Third Peoples Hospital Of Jinan City | Ren C.,The Third Peoples Hospital Of Jinan City | And 2 more authors.
Tumor Biology | Year: 2015

The high mobility group A2 (HMGA2), an oncofetal protein, was shown to play a role in tumor development and progression. However, the molecular and clinical role of HMGA2 in epithelial ovarian carcinomas (EOCs) is still unknown. In the present study, EOC cell line SKOV3 was subjected to in vitro assays. Here, our findings showed that HMGA2 was highly expressed in EOC cell line SKOV3. HMGA2 knockdown promoted cell apoptosis and the cleavage of caspase 3, and decreased the B cell lymphoma 2 (Bcl-2)/Bax ratio in SKOV3. Functionally, HMGA2 knockdown resulted in reduction of SKOV3 cell migration and invasion. Mechanically, HMGA2 knockdown affected the occurrence of EMT by increasing E-cadherin gene and protein expression and decreasing the gene and protein expression of N-cadherin, slug, and vimentin. At the same time, HMGA2 also repressed the expression of matrix metalloproteinase 2 (MMP2) and matrix metalloproteinase 9 (MMP9), which was consistent with the decreased invasion capacity. In conclusion, HMGA2 is associated with migration and invasiveness and regulates the progression of EMT in the development of EOC, and HMGA2 gene and protein may be a novel therapeutic target against EOC in the clinical practice. © 2015 International Society of Oncology and BioMarkers (ISOBM)


PubMed | The Third Peoples Hospital of Jinan City and Shandong Academy of Sciences
Type: Journal Article | Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine | Year: 2016

The high mobility group A2 (HMGA2), an oncofetal protein, was shown to play a role in tumor development and progression. However, the molecular and clinical role of HMGA2 in epithelial ovarian carcinomas (EOCs) is still unknown. In the present study, EOC cell line SKOV3 was subjected to in vitro assays. Here, our findings showed that HMGA2 was highly expressed in EOC cell line SKOV3. HMGA2 knockdown promoted cell apoptosis and the cleavage of caspase 3, and decreased the B cell lymphoma 2 (Bcl-2)/Bax ratio in SKOV3. Functionally, HMGA2 knockdown resulted in reduction of SKOV3 cell migration and invasion. Mechanically, HMGA2 knockdown affected the occurrence of EMT by increasing E-cadherin gene and protein expression and decreasing the gene and protein expression of N-cadherin, slug, and vimentin. At the same time, HMGA2 also repressed the expression of matrix metalloproteinase 2 (MMP2) and matrix metalloproteinase 9 (MMP9), which was consistent with the decreased invasion capacity. In conclusion, HMGA2 is associated with migration and invasiveness and regulates the progression of EMT in the development of EOC, and HMGA2 gene and protein may be a novel therapeutic target against EOC in the clinical practice.


PubMed | The Third Peoples Hospital of Jinan City and Shandong Academy of Sciences
Type: Journal Article | Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine | Year: 2016

Nuclear protein C23 and epidermal growth factor receptor (EGFR) are reported to be correlated with cervical cancer (CC). However the correlations between C23 and EGFR were rarely reported. Here, this study explored the effects of C23 in activation of EGFR signaling pathway. In our study, immunohistochemistry was used to identify the expression of C23 or EGFR in CC tissues. The level of the phosphorylated EGFR was observed by western blot, and cell invasion capacity was detected by Transwell assay. In this study, we found that C23 and EGFR were highly expressed in cervical cancer tissues, while C23 on the cell surface mainly expressed in CC tissues with lymph node metastasis, and was correlated to EGFR statistically. In vitro, western blot showed that either anti-C23 or anti-EGFR antibodies can inhibit the phosphorlation of EGFR with significant differences (p<0.01). Besides, based on Transwell assay, the number of membrane-invading cells was reduced significantly in anti-C23 group, and no significant difference was found compared with anti-EGFR treatment (p>0.05). In conclusion, C23 on the cell surface may be a kind of indispensable component in activation of EGFR signaling, by which C23 can participate in the growth and invasion of tumors. C23 antagonists may provide a new field for cervical cancer therapy.


PubMed | The Third Peoples Hospital of Jinan City and Shandong Academy of Sciences
Type: Journal Article | Journal: Molecular neurobiology | Year: 2016

Rab31, a member of the Ras superfamily, is reported to play a role in tumor development and progression. However, the detailed role of Rab31 in proliferation and apoptosis of cancer cells is still unclear. Here, we used different cell lines, such as glioblastoma, and cervical cancer, to investigate the role of Rab31 in cancer progression. We found that Rab31 promotes U87 and SiHa cell proliferation via activation of G1/S checkpoint transitions, accompanied with an increase of cyclin D1, cyclin A, and cyclin B1. Meanwhile, Rab31 inhibits U87 and SiHa cell apoptosis, and decreased the BAX and PIG3 expression, but enhanced BCL2 expression. In addition, Rab31 induces N-cadherin, Vimentin, and Snail expression, and inhibits E-cadherin expression to regulate proliferation and migration. Besides, we observed that ERK1/2 and PI3k/AKT pathways are required for Rab31-induced cell proliferation and migration. In vivo, the knockdown of Rab31 suppresses tumor mass growth. In conclusion, our data highlight the crucial role of Rab31 in cancer progression, proliferation, and apoptosis, and indicates that Rab31 may be a useful and effective target for the clinical therapy of most cancers.

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