Hepatoma-Derived Growth Factor and DDX5 Promote Carcinogenesis and Progression of Endometrial Cancer by Activating β-Catenin

Liu, Chunhua; Wang, Lijing; Jiang, Qingping; Zhang, Junyi; Zhu, Liqiong; Lin, Li; Jiang, Huiping; Lin, Dan; Xiao, Yanyi; Fang, Weiyi; Guo, Suiqun

doi:10.3389/fonc.2019.00211

Cited by 28 publications

(29 citation statements)

References 48 publications

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“…HDGF was originally obtained from the conditioned media of HuH-7 hepatoma cells [ 19 ]. It has been widely reported as an oncogenic factor promoting tumor pathogenesis including nonsmall cell lung carcinoma (NSCLC), endometrial cancer, nasopharyngeal carcinoma, breast cancer, and liver cancer in previous studies [ 20 – 25 ]. In a recent study, Wang et al found that methyltransferase-like 3 (METTL3) mediated m(6)A modification of HDGF mRNA and increased its mRNA stability.…”

Section: Discussionmentioning

confidence: 99%

NAP1L1 interacts with hepatoma-derived growth factor to recruit c-Jun inducing breast cancer growth

et al. 2021

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Background Breast cancer is a common cancer among women in the world. However, its pathogenesis is still to be determined. The role and molecular mechanism of Nucleosome Assembly Protein 1 Like 1 (NAP1L1) in breast cancer have not been reported. Elucidation of molecular mechanism might provide a novel therapeutic target for breast cancer treatment. Methods A bioinformatics analysis was conducted to determine the differential expression of NAP1L1 in breast cancer and find the potential biomarker that interacts with NAP1L1 and hepatoma-derived growth factor (HDGF). The expression of NAP1L1 in tissues was detected by using immunohistochemistry. Breast cancer cells were transfected with the corresponding lentiviral particles and siRNA. The efficiency of transfection was measured by RT-qPCR and western blotting. Then, MTT, Edu, plate clone formation, and subcutaneous tumorigenesis in nude mice were used to detect the cell proliferation in breast cancer. Furthermore, coimmunoprecipitation (Co-IP) assay and confocal microscopy were performed to explore the detailed molecular mechanism of NAP1L1 in breast cancer. Results In this study, NAP1L1 protein was upregulated based on the Clinical Proteomic Tumor Analysis Consortium (CPTAC) database. Consistent with the prediction, immunohistochemistry staining showed that NAP1L1 protein expression was significantly increased in breast cancer tissues. Its elevated expression was an unfavorable factor for breast cancer clinical progression and poor prognosis. Stably or transiently knocking down NAP1L1 reduced the cell growth in vivo and in vitro via repressing the cell cycle signal in breast cancer. Furthermore, the molecular basis of NAP1L1-induced cell cycle signal was further studied. NAP1L1 interacted with the HDGF, an oncogenic factor for tumors, and the latter subsequently recruited the key oncogenic transcription factor c-Jun, which finally induced the expression of cell cycle promoter Cyclin D1(CCND1) and thus the cell growth of breast cancer. Conclusions Our data demonstrated that NAP1L1 functions as a potential oncogene via interacting with HDGF to recruit c-Jun in breast cancer.

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Section: Discussionmentioning

confidence: 99%

NAP1L1 interacts with hepatoma-derived growth factor to recruit c-Jun inducing breast cancer growth

et al. 2021

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“…T24 and 253J cells were digested with trypsin (Gibco, USA) and dissociated repeatedly to prepare a single cell suspension. Migration assays were performed as described previously 20. After rubbing away the cells failed to through the membrane and washing with PBS three times, these chambers were photographed using an upright fluorescence microscope.…”

Section: Methodsmentioning

confidence: 99%

Downregulation of HDGF inhibits the tumorigenesis of bladder cancer cells by inactivating the PI3K-AKT signaling pathway

Zhang¹,

Chang²,

Chen³

et al. 2019

CMAR

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BackgroundHepatoma-derived growth factor (HDGF) is a heparin-binding protein that has been observed to be abnormally expressed in numerous malignancies, but the definite role of HDGF in bladder cancer (BCa) has not been clarified. Here, we conduct the present study to evaluate correlations between HDGF and BCa.MethodsBioinformatics analysis was used to evaluate HDGF expression levels in BCa tissues. The effect of HDGF on cell proliferation, migration, invasion, cell cycle and apoptosis was analyzed utilizing CCK-8, clone formation, Transwell assays and flow cytometry, respectively. In addition, the xenograft tumor model was established.ResultsBased on bioinformatics analysis, we noticed that HDGF was highly expressed in BCa tissues and was positively correlated with poor prognosis in patients. Knockdown of HDGF markedly reduced tumorigenesis in BCa cells. Furthermore, the results of flow cytometry showed that HDGF deletion enhanced apoptosis in T24 and 253J cells and led to cell cycle arrest in G1 phase. In further studies, we found that tumor growth was inhibited in xenograft nude mouse models with HDGF deletion. The results of RNA-seq analysis revealed that the PI3K-AKT signaling pathway-related genes were obviously changed in HDGF-deficient 253J cells, and this result was further confirmed by Western blot analysis.ConclusionIn summary, we suggest that HDGF plays a substantial role in BCa and promotes tumor development and progression by regulating the PI3K-AKT signaling pathway, which provides a promising target for BCa treatment.

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“…Previous studies have reported the involvement of HDGF in the regulation of the WNT/β-catenin pathway. [32][33][34] Accordingly, we tested whether miR-939 affects WNT/βcatenin signaling in PCa. To this end, we conducted Western blotting to quantify the important molecules associated with the WNT/β-catenin pathway in DU145 and PC3 cells transfected with agomir-939 in the presence of either pc-HDGF or pcDNA3.1.…”

Section: Mir-939 Overexpression Deactivates the Wnt/β-catenin Pathwaymentioning

confidence: 99%

MicroRNA-939 Directly Targets HDGF to Inhibit the Aggressiveness of Prostate Cancer via Deactivation of the WNT/β-Catenin Pathway

Song¹,

Zhang²,

Zi³

et al. 2020

OTT

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MicroRNA-939 (miR-939) has crucial roles in several types of human cancer. However, the expression profile and precise functions of miR-939 in prostate cancer (PCa) are still unclear. This study aimed to determine miR-939 expression in PCa and explore its roles in PCa tumorigenesis. Methods: miR-939 expression was determined in PCa tissues and cell lines using reverse transcription-quantitative polymerase chain reaction. Cell Counting Kit-8, colony formation, and flow cytometric assays were used to determine the role of miR-939 in PCa cell proliferation and apoptosis in vitro, whereas a tumor xenograft model was generated to evaluate the effect of miR-939 on tumor growth in vivo. Transwell assays were performed to investigate whether miR-939 affects the migration and invasiveness of PCa cells. Results: miR-939 was found to be downregulated in PCa tissues and cell lines, and this downregulation was significantly correlated with tumor stage and lymphatic metastasis. Patients with PCa exhibiting low miR-939 expression had shorter overall survival than those exhibiting high miR-939 expression. Exogenous miR-939 expression suppressed PCa cell proliferation, colony formation, migration, and invasion in vitro; enhanced apoptosis in vitro; and decreased tumor growth in vivo. Investigation of the underlying molecular mechanisms revealed hepatoma-derived growth factor (HDGF) as a direct target gene of miR-939 in PCa. HDGF was found to be significantly upregulated in PCa tissues, and its expression was inversely correlated with miR-939 expression. HDGF silencing and miR-939 upregulation showed similar effects in PCa. Restored HDGF expression counteracted the tumor-suppressive activity of miR-939 overexpression in PCa cells. Furthermore, ectopic miR-939 expression inhibited the WNT/β-catenin pathway activation in PCa both in vitro and in vivo by downregulating HDGF. Conclusion: miR-939 functions as a tumor suppressor during PCa tumorigenesis by directly targeting HDGF and deactivating the WNT/β-catenin pathway, suggesting the miR-939/ HDGF/WNT/β-catenin pathway as an effective target for PCa therapy.

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Hepatoma-Derived Growth Factor and DDX5 Promote Carcinogenesis and Progression of Endometrial Cancer by Activating β-Catenin

Cited by 28 publications

References 48 publications

NAP1L1 interacts with hepatoma-derived growth factor to recruit c-Jun inducing breast cancer growth

NAP1L1 interacts with hepatoma-derived growth factor to recruit c-Jun inducing breast cancer growth

<p>Downregulation of HDGF inhibits the tumorigenesis of bladder cancer cells by inactivating the PI3K-AKT signaling pathway</p>

<p>MicroRNA-939 Directly Targets <em>HDGF</em> to Inhibit the Aggressiveness of Prostate Cancer via Deactivation of the WNT/β-Catenin Pathway</p>

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