Longyang Liu

Expression and clinical value of EIF3CL in serous ovarian cancer

Objectives This study aimed to explore the expression of eukaryotic translation initiation factor 3 subunit C-like in serous ovarian cancer samples (both paraffin-embedded and fresh samples) and evaluate its clinical value in patients with serous ovarian cancer. Methods Twenty-five fresh serous ovarian cancer tissues and their paired paratumor tissues were subjected to reverse transcription–quantitative polymerase chain reaction assay to detect eukaryotic translation initiation factor 3 subunit C-like messenger RNA expression. In addition, 135 paraffin-embedded serous ovarian cancer samples and 36 paratumor samples were assessed for eukaryotic translation initiation factor 3 subunit C-like protein expression using immunohistochemistry. Results Both protein and messenger RNA expression levels of eukaryotic translation initiation factor 3 subunit C-like were higher in serous ovarian cancer samples than in paratumor samples, and its high expression was associated with poor overall survival in patients with serous ovarian cancer. In addition, multivariate Cox regression analysis showed that high expression of eukaryotic translation initiation factor 3 subunit C-like was an independent poor prognostic factor for patients with serous ovarian cancer. Conclusions Eukaryotic translation initiation factor 3 subunit C-like is upregulated in serous ovarian cancer samples, and it may be recommended as a useful poor prognostic biomarker in patients with serous ovarian cancer.

Retracted: MYH10 Combines with MYH9 to Recruit USP45 by Deubiquitinating Snail and Promotes Serous Ovarian Cancer Carcinogenesis, Progression, and Cisplatin Resistance

Abstract The poor prognosis of serous ovarian cancer (SOC) is due to its high invasive capacity and cisplatin resistance of SOC cells, whereas the molecular mechanisms remain poorly understood. In the present study, the expression and function of non‐muscle myosin heavy chain IIB (MYH10) in SOC are identified by immunohistochemistry, in vitro, and in vivo studies, respectively. The mechanism of MYH10 is demonstrated by co‐immunoprecipitation, GST pull‐down, confocal laser assays, and so on. The results show that the knockdown of MYH10 suppressed SOC cell proliferation, migration, invasion, metastasis, and cisplatin resistance both in vivo and in vitro. Further studies confirm that the MYH10 protein functional domain combines with non‐muscle myosin heavy chain IIA (MYH9) to recruit the deubiquitinating enzyme Ubiquitin‐specific proteases 45 and deubiquitinates snail to inhibit snail degradation, eventually promoting tumorigenesis, progression, and cisplatin resistance in SOC. In clinical samples, MYH10 expression is significantly elevated in SOC samples compared to the paratumor samples. And the expression of MYH10 is positively correlated with MYH9 expression. MYH10+/MYH9+ co‐expression is an independent prognostic factor for predicting SOC patient survival. These findings uncover a key role of the MYH10‐MYH9‐snail axis in SOC carcinogenesis, progression, and cisplatin resistance, and provide potential novel therapeutic targets for SOC intervention.

VPS33B interacts with NESG1 to suppress cell growth and cisplatin chemoresistance in ovarian cancer

Abstract The pathogenesis and cisplatin chemoresistance of ovarian cancer (OC) are still unclear. Vacuolar protein sorting‐associated 33B (VPS33B) has not been reported in OC to date. In this study, immunohistochemistry was used to detect VPS33B protein expression between OC and ovarian tissues. MTT, EdU, colony formation, cell cycle, in vivo tumorigenesis, western blot, ChIP, EMSA, co‐immunoprecipitation (CoIP), qRT‐PCR, and microconfocal microscopy were used to explore the function and molecular mechanisms of VPS33B in OC cells. The results of the present study demonstrated that VPS33B protein expression was obviously reduced in OC compared with that in ovarian tissues. Overexpressed VPS33B suppressed cell cycle transition, cell growth, and chemoresistance to cisplatin in vitro and in vivo. Analysis of the mechanism indicated that overexpressed VPS33B regulated the epidermal growth factor receptor (EGFR)/PI3K/AKT/c‐Myc/p53/miR‐133a‐3p feedback loop and reduced the expression of the cell cycle factor CDK4. Nasopharyngeal epithelium‐specific protein 1 (NESG1) as a tumor suppressor not only interacted with VPS33B, but was also induced by VPS33B by the attenuation of PI3K/AKT/c‐Jun‐mediated transcription inhibition. Overexpressed NESG1 further suppressed cell growth by mediating VPS33B‐modulated signals in VPS33B‐overexpressing OC cells. Finally, NESG1 induced VPS33B expression by reducing the inhibition of PI3K/AKT/c‐Jun‐mediated transcription. Our study is the first to demonstrate that VPS33B serves as a tumor suppressor, and VPS33B can interact with NESG1 to suppress cell growth and promote cisplatin sensitivity by regulating the EGFR/PI3K/AKT/c‐Myc/p53/miR‐133a‐3p feedback loop in OC cells.

Expression and Clinical Significance of Microtubule-Actin Cross-Linking Factor 1 in Serous Ovarian Cancer

Background: Ovarian Cancer (OC) remains the first leading cause of gynecologic malignancy. The survival rate from Serous Ovarian Cancer (SOC) is very low, and the present prognostic predictors of SOC are not very sensitive or specific. Objective: The present study aimed to investigate Microtubule-Actin Cross-Linking Factor 1 (MACF1) expression in SOC tissues (including paraffin-embedded and fresh tissues) and to assess its expression and significant value in patients with SOC. Methods: A total of 18 fresh SOC tissues and their paired paratumor tissues were performed with reverse-transcription quantitative PCR analysis to detect MACF1 mRNA expression. Moreover, 175 paraffin embedded SOC tissues and 41 paratumor tissues were assessed for MACF1 expression using immunohistochemistry. Results: The mRNA and protein expression of MACF1 were both higher in cancer tissues than that in paratumor tissues, and MACF1 high expression was associated with shorter Recurrence Free Survival (RFS) and Overall Survival (OS) in patients with SOC. Furthermore, multivariate regression analysis showed that high MACF1 expression was an independent poor survival predictor of patients with SOC. Conclusion: MACF1 is upregualted in SOC, and it may be used as a useful patent of prognostic biomarker in SOC.