TRIM59 Is a Novel Marker of Poor Prognosis and Promotes Malignant Progression of Ovarian Cancer by Inducing Annexin A2 Expression

Abstract Background: Homeobox B4 (HOXB4) is associated with the poor prognosis of various cancer types. However, how HOXB4 promotes ovarian cancer (OV) progression remains to be determined. Methods：The Cancer Genome Atlas (TCGA) database indicated that high level of HOXB4 in OV was correlated with poor prognosis. The biological functions of HOXB4 were confirmed through a colony formation, migration, and invasion assay. The effect of HOXB4 on the expression of EMT and cancer stem cell markers was detected. The transcriptional target of HOXB4 was DHDDS, which was detected by a ChIP assay. A xenograft tumor model was performed in nude mice to detect the role of HOXB4 in tumor proliferation and metastasis. Results：Results showed that the expression of HOXB4 was higher in OV tissues than in normal tissues and correlated with the poor prognosis of OV. HOXB4 knockdown suppressed the proliferation and invasion ability of OV cells in vitro. Conversely, these effects were enhanced by the up-regulation of HOXB4 in OV cells. The binding of two DNA motifs through HOXB4 regulated DHDDS expression and contributed to the malignant progression of OV. The role of HOXB4 in promoting tumor proliferation and metastasis was verified in mice. Further investigation revealed that HOXB4 triggered Snail and Zeb1 expression. Conclusion: Overall, HOXB4 overexpression was remarkably correlated with the poor prognosis of OV. HOXB4 up-regulated DHDDS, which co-contributed to the enhancer proliferation and invasion of OV cells, thus accelerating the malignant progression of OV.

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Upregulation of SNHG3 expression associated with poor prognosis and enhances malignant progression of ovarian cancer

Cancer Biomarkers ◽

10.3233/cbm-170710 ◽

2018 ◽

Vol 22 (3) ◽

pp. 367-374 ◽

Cited By ~ 18

Author(s):

Lan Hong ◽

Wangsheng Chen ◽

Dongcai Wu ◽

Yifeng Wang

Keyword(s):

Ovarian Cancer ◽

Poor Prognosis ◽

Malignant Progression

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Co‑expression of Lewis�y antigen and CD147 in�epithelial ovarian cancer is correlated with malignant progression and poor prognosis

International Journal of Molecular Medicine ◽

10.3892/ijmm.2019.4103 ◽

2019 ◽

Author(s):

Juanjuan Liu ◽

Qi Liu ◽

Yanyan Wang ◽

Miao Liu ◽

Yue Qi ◽

...

Keyword(s):

Ovarian Cancer ◽

Epithelial Ovarian Cancer ◽

Poor Prognosis ◽

Malignant Progression ◽

Lewis Y Antigen ◽

Lewis Y

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HOXB4 promotes the malignant progression of ovarian cancer via DHDDS

10.21203/rs.2.18907/v3 ◽

2020 ◽

Author(s):

Na Li ◽

Jin-hai Gou ◽

Jiao Xiong ◽

Juan-juan You ◽

Zhengyu Li

Keyword(s):

Ovarian Cancer ◽

Poor Prognosis ◽

Tumor Model ◽

Malignant Progression ◽

The Cancer Genome Atlas ◽

Migration And Invasion ◽

Proliferation And Invasion

Abstract Background : Homeobox B4 (HOXB4) is correlated with poor prognosis of various cancer types. However, how HOXB4 promotes ovarian cancer (OV) progression remains unclear. Methods : The Cancer Genome Atlas (TCGA) database indicated that a high level of HOXB4 in OV was correlated with poor prognosis. The biological functions of HOXB4 were confirmed by colony formation, migration, and invasion assays. The effect of HOXB4 on the expression of EMT cell markers was determined. The transcriptional target of HOXB4 was DHDDS, which was detected by a ChIP assay. A xenograft tumor model was generated in nude mice to detect the role of HOXB4 in tumor proliferation and metastasis. Results : The results showed that HOXB4 protein levels were higher in OV tissues than in normal tissues and correlated with poor prognosis of OV. HOXB4 reduction inhibited the proliferation and invasion ability of OV cells in vitro. Conversely, these effects were enhanced by the upregulation of HOXB4 in OV cells. The binding of HOXB4 to two DNA motifs regulated DHDDS expression and contributed to the malignant progression of OV. The role of HOXB4 in contributing to tumor development in vivo was verified in mice. Further results indicated that HOXB4 induced Snail and Zeb1 expression. Conclusion : Overall, HOXB4 overexpression was remarkably correlated with poor prognosis of OV. Mechanistically, HOXB4 enhances the proliferation and invasion of tumor cells by activating DHDDS, thereby promoting the malignant progression of OV.

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HOXB4 promotes the malignant progression of ovarian cancer via DHDDS

10.21203/rs.2.18907/v2 ◽

2020 ◽

Author(s):

Na Li ◽

Jiao Xiong ◽

Zhengyu Li

Keyword(s):

Ovarian Cancer ◽

Poor Prognosis ◽

Tumor Model ◽

Malignant Progression ◽

The Cancer Genome Atlas ◽

Migration And Invasion ◽

Proliferation And Invasion

Abstract Background : Homeobox B4 (HOXB4) is correlated with poor prognosis of various cancer types. However, how HOXB4 promotes ovarian cancer (OV) progression remains unclear. Methods : The Cancer Genome Atlas (TCGA) database indicated that a high level of HOXB4 in OV was correlated with poor prognosis. The biological functions of HOXB4 were confirmed by colony formation, migration, and invasion assays. The effect of HOXB4 on the expression of EMT cell markers was determined. The transcriptional target of HOXB4 was DHDDS, which was detected by a ChIP assay. A xenograft tumor model was generated in nude mice to detect the role of HOXB4 in tumor proliferation and metastasis. Results : The results showed that HOXB4 protein levels were higher in OV tissues than in normal tissues and correlated with poor prognosis of OV. HOXB4 reduction inhibited the proliferation and invasion ability of OV cells in vitro. Conversely, these effects were enhanced by the upregulation of HOXB4 in OV cells. The binding of HOXB4 to two DNA motifs regulated DHDDS expression and contributed to the malignant progression of OV. The role of HOXB4 in contributing to tumor development in vivo was verified in mice. Further results indicated that HOXB4 induced Snail and Zeb1 expression. Conclusion : Overall, HOXB4 overexpression was remarkably correlated with poor prognosis of OV. Mechanistically, HOXB4 enhances the proliferation and invasion of tumor cells by activating DHDDS, thereby promoting the malignant progression of OV.

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LONG NON-CODING RNA AHIF PREDICTS POOR PROGNOSIS IN EPITHELIAL OVARIAN CANCER AND AFFECTS CELL PROLIFERATION THROUGH THE REGULATION OF CELL CYCLE, APOPTOSIS AND SENESCENCE

10.26226/morressier.5770e29cd462b80290b4c0f3 ◽

2016 ◽

Author(s):

junjun qiu

Keyword(s):

Cell Cycle ◽

Ovarian Cancer ◽

Cell Proliferation ◽

Epithelial Ovarian Cancer ◽

Poor Prognosis ◽

Non Coding Rna ◽

Regulation Of Cell Cycle ◽

Long Non Coding Rna

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GENE CO-EXPRESSION NETWORK ANALYSIS REVEALS NECTIN 4 AS NEW THERAPEUTIC TARGET FOR A POOR-PROGNOSIS SUBTYPE OF OVARIAN CANCER

10.26226/morressier.597eedbdd462b80296ca1a2f ◽

2017 ◽

Author(s):

Pils Dietmar

Keyword(s):

Ovarian Cancer ◽

Network Analysis ◽

Therapeutic Target ◽

Poor Prognosis

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Prognostic significance of bone marrow FDG uptake in patients with gynecological cancer

Scientific Reports ◽

10.1038/s41598-021-81298-1 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Kotaro Shimura ◽

Seiji Mabuchi ◽

Naoko Komura ◽

Eriko Yokoi ◽

Katsumi Kozasa ◽

...

Keyword(s):

Ovarian Cancer ◽

Bone Marrow ◽

Poor Prognosis ◽

Gynecological Cancer ◽

Prognostic Significance ◽

Standardized Uptake Value ◽

Suppressor Cells ◽

Underlying Mechanism ◽

Fdg Uptake

AbstractWe investigated the prognostic significance and the underlying mechanism of increased bone marrow (BM) 2-(18F) fluoro-2-deoxy-D-glucose as a tracer (FDG)-uptake in patients with gynecological cancer. A list of patients diagnosed with cervical, endometrial, and ovarian cancer from January 2008 to December 2014 were identified. Then, through chart reviews, 559 patients who underwent staging by FDG-positron emission tomography (PET)/computed tomography (CT) and subsequent surgical resection were identified, and their clinical data were reviewed retrospectively. BM FDG-uptake was evaluated using maximum standardized uptake value (SUVmax) and BM-to-aorta uptake ratio (BAR). As a result, we have found that increased BAR was observed in 20 (8.7%), 21 (13.0%), 21 (12.6%) of cervical, endometrial, and ovarian cancer, respectively, and was associated with significantly shorter survival. Increased BAR was also closely associated with increased granulopoiesis. In vitro and in vivo experiments revealed that tumor-derived granulocyte colony-stimulating factor (G-CSF) was involved in the underlying causative mechanism of increased BM FDG-uptake, and that immune suppression mediated by G-CSF-induced myeloid-derived suppressor cells (MDSCs) is responsible for the poor prognosis of this type of cancer. In conclusion, increased BM FDG-uptake, as represented by increased BAR, is an indicator of poor prognosis in patients with gynecological cancer.

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A novel homeostatic loop of sorcin drives paclitaxel-resistance and malignant progression via Smad4/ZEB1/miR-142-5p in human ovarian cancer

Oncogene ◽

10.1038/s41388-021-01891-6 ◽

2021 ◽

Author(s):

Jinguo Zhang ◽

Wencai Guan ◽

Xiaolin Xu ◽

Fanchen Wang ◽

Xin Li ◽

...

Keyword(s):

Ovarian Cancer ◽

Calcium Binding ◽

Molecular Mechanisms ◽

Epithelial Mesenchymal Transition ◽

Malignant Progression ◽

Bioinformatics Analyses ◽

Aberrant Expression ◽

Mesenchymal Transition ◽

E Box

AbstractThe primary chemotherapy of ovarian cancer (OC) often acquires chemoresistance. Sorcin (SRI), a soluble resistance-related calcium-binding protein, has been reported to be an oncogenic protein in cancer. However, the molecular mechanisms of SRI regulation and the role and aberrant expression of SRI in chemoresistant OC remain unclear. Here, we identified SRI as a key driver of paclitaxel (PTX)-resistance and explored its regulatory mechanism. Using transcriptome profiles, qRT-PCR, proteomics, Western blot, immunohistochemistry, and bioinformatics analyses, we found that SRI was overexpressed in PTX-resistant OC cells and the overexpression of SRI was related to the poor prognosis of patients. SRI was a key molecule required for growth, migration, and PTX-resistance in vitro and in vivo and was involved in epithelial–mesenchymal transition (EMT) and stemness. Mechanistic studies showed that miR-142-5p directly bound to the 3ʹ-UTR of SRI to suppress its expression, whereas a transcription factor zinc-finger E-box binding homeobox 1 (ZEB1) inhibited the transcription of miR-142-5p by directly binding to the E-box fragment in the miR-142 promoter region. Furthermore, ZEB1 was negatively regulated by SRI which physically interacted with Smad4 to block its translocation from the cytosol to the nucleus. Taken together, our findings unveil a novel homeostatic loop of SRI that drives the PTX-resistance and malignant progression via Smad4/ZEB1/miR-142-5p in human OC. Targeting this SRI/Smad4/ZEB1/miR-142-5p loop may reverse the PTX-resistance.

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