9L Gliosarcoma Cell Proliferation and Tumor Growth in Rats Are Suppressed by N-Hydroxy-N′-(4-butyl-2-methylphenol) Formamidine (HET0016), a Selective Inhibitor of CYP4A

Abstract Objective Dysregulation of KLF7 participates in the development of various cancers, but it is unclear whether there is a link between HCC and aberrant expression of KLF7. The aim of this study was to investigate the role of KLF7 in proliferation and migration of hepatocellular carcinoma (HCC) cells. Methods CCK8, colony growth, transwell, cell cycle analysis and apoptosis detection were performed to explore the effect of KLF7, VPS35 and Ccdc85c on cell function in vitro. Xenografted tumor growth was used to assess in vivo role of KLF7. Chip-qPCR and luciferase reporter assays were applied to check whether KLF7 regulated VPS35 at transcriptional manner. Co-IP assay was performed to detect the interaction between VPS35 and Ccdc85c. Immunohistochemical staining and qRT-PCR analysis were performed in human HCC sampels to study the clinical significance of KLF7, VPS35 and β-catenin. Results Firstly, KLF7 was highly expressed in human HCC samples and correlated with patients’ differentiation and metastasis status. KLF7 overexpression contributed to cell proliferation and invasion of HCC cells in vitro and in vivo. KLF7 transcriptional activation of VPS35 was necessary for HCC tumor growth and metastasis. Further, co-IP studies revealed that VPS35 could interact with Ccdc85c in HCC cells. Rescue assay confirmed that overexpression of VPS35 and knockdown of Ccdc85c abolished the VPS35-medicated promotion effect on cell proliferation and invasion. Finally, KLF7/VPS35 axis regulated Ccdc85c, which involved in activation of β-catenin signaling pathway, confirmed using β-catenin inhibitor, GK974. Functional studies suggested that downregulation of Ccdc85c partly reversed the capacity of cell proliferation and invasion in HCC cells, which was regulated by VPS35 upregulation. Lastly, there was a positive correlation among KLF7, VPS35 and active-β-catenin in human HCC patients. Conclusion We demonstrated that KLF7/VPS35 axis promoted HCC cell progression by activating Ccdc85c-medicated β-catenin pathway. Targeting this signal axis might be a potential treatment strategy for HCC.

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Circ_002059 suppresses cell proliferation and migration of gastric cancer via miR-182/MTSS1 axis

Acta Biochimica et Biophysica Sinica ◽

10.1093/abbs/gmab015 ◽

2021 ◽

Vol 53 (4) ◽

pp. 454-462

Author(s):

Ting Li ◽

Xiaomin Zuo ◽

Xiangling Meng

Keyword(s):

Gastric Cancer ◽

Cell Proliferation ◽

Tumor Growth ◽

Luciferase Reporter ◽

Metastasis Suppressor ◽

Xenograft Tumor ◽

Cell Proliferation And Migration ◽

And Migration ◽

Xenograft Tumor Growth ◽

Proliferation And Migration

Abstract Circular RNAs (circRNAs) play either oncogenic or tumor suppressive roles in gastric cancer (GC). A previous study demonstrated that circ_002059, a typical circRNA, was downregulated in GC tissues. However, the role and mechanism of circ_002059 in GC development are still unknown. In this study, the levels of circ_002059, miR-182, and metastasis suppressor-1 (MTSS1) were examined by real-time quantitative polymerase chain reaction and western blot analysis. Cell proliferation and migration were evaluated by MTT assay and Transwell migration assay, respectively. The interactions between miR-182 and circ_002059 or MTSS1 were analyzed by dual-luciferase reporter assay. A GC xenograft model was established to validate the role of circ_002059 in GC progression in vivo. Overexpression of circ_002059 significantly inhibited, whereas knockdown of circ_002059 notably facilitated, cell proliferation and migration in GC cells. MTSS1 was found to be a direct target of miR-182 and circ_002059 upregulated MTSS1 expression by competitively sponging miR-182. Transfection with miR-182 mimic and MTSS1 silencing abated the inhibitory effect of circ_002059 on GC progression. Circ_002059 inhibited GC cell xenograft tumor growth by regulating miR-182 and MTSS1 expression. Collectively, Circ_002059 inhibited GC cell proliferation and migration in vitro and xenograft tumor growth in mice, by regulating the miR-182/MTSS1 axis.

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The ubiquitin ligase HERC4 mediates c-Maf ubiquitination and delays the growth of multiple myeloma xenografts in nude mice

Blood ◽

10.1182/blood-2015-07-658203 ◽

2016 ◽

Vol 127 (13) ◽

pp. 1676-1686 ◽

Cited By ~ 20

Author(s):

Zubin Zhang ◽

Jiefei Tong ◽

Xiaowen Tang ◽

Jiaxiang Juan ◽

Biyin Cao ◽

...

Keyword(s):

Multiple Myeloma ◽

Cell Proliferation ◽

Tumor Growth ◽

Ubiquitin Ligase ◽

Nude Mice ◽

Key Points

Key Points HERC4 is the first identified ubiquitin ligase that mediates c-Maf ubiquitination and degradation. HERC4 suppresses MM cell proliferation and delays MM tumor growth.

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MicroRNA-297b-5p/3p target Mllt3/Af9 to suppress lymphoma cell proliferation, migration and invasionin vitroand tumor growth in nude mice

Leukemia & Lymphoma ◽

10.3109/10428194.2012.678005 ◽

2012 ◽

Vol 53 (10) ◽

pp. 2033-2040 ◽

Cited By ~ 9

Author(s):

Tiantian Zhang ◽

Yu Luo ◽

Tao Wang ◽

James Y. Yang

Keyword(s):

Cell Proliferation ◽

Tumor Growth ◽

Nude Mice ◽

Lymphoma Cell

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Increased expression of MAP2 inhibits melanoma cell proliferation, invasion and tumor growth in vitro and in vivo

Experimental Dermatology ◽

10.1111/j.1600-0625.2009.01020.x ◽

2010 ◽

Vol 19 (11) ◽

pp. 958-964 ◽

Cited By ~ 8

Author(s):

Zhiqi Song ◽

Chun-Di He ◽

Changkai Sun ◽

Yanni Xu ◽

Xin Jin ◽

...

Keyword(s):

Cell Proliferation ◽

Tumor Growth ◽

Melanoma Cell ◽

Melanoma Cell Proliferation

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LncRNA SNHG14 Promotes Progression of Ovarian Cancer by Regulating miR-206 Expression

Tobacco Regulatory Science ◽

10.18001/trs.7.5.1.174 ◽

2021 ◽

Vol 7 (5) ◽

pp. 3997-4004

Author(s):

Zhibo Zou ◽

Lin Peng

Keyword(s):

Ovarian Cancer ◽

Flow Cytometry ◽

Cell Proliferation ◽

Tumor Growth ◽

Cancer Progression ◽

Nude Mice ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Qrt Pcr ◽

Research Objects

Objective: This study aimed to probe into the effect of LncRNA SNHG14 on ovarian cancer progression by regulating miR-206.Methods: Fifty-seven ovarian cancer (OC) patients who were treated in our hospital from December 2017 to December 2019 were collected as the research objects. During the operation, OC tissues and paracancerous tissues of patients were collected, and the effect of SNHG14 on OC tumor growth in nude mice was detected, and SNHG14 inhibitor was transfected into OC cells. The relative expression of SNHG14 in tissues and cells was detected by qRT-PCR, cell proliferation was testedvia CCK8, migration and invasion were detected through Transwell, apoptosis was assessedvia flow cytometry, and the targeted relationship between SNHG14 and miR-206 was detected by dual luciferase reporter gene.Results: SNHG14 is highly expressed in OC tissues, cells and nude mice. Down-regulating it can inhibit the biological ability of OC cells and inhibit the growth of nude mice tumors. It can directly target miR-206 to regulate CCND1 expression and promote OC progression.Conclusion: LncRNA SNHG14 can act as miR-206 sponge to regulate CCND1 expression downstream of miR-206 and promote OC progression.

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Hsa_circ_0023990 Promotes Tumor Growth and Glycolysis in Dedifferentiated TC via Targeting miR-485-5p/FOXM1 Axis

Endocrinology ◽

10.1210/endocr/bqab172 ◽

2021 ◽

Vol 162 (12) ◽

Author(s):

Qing Zhang ◽

Lian Wu ◽

Shao-Zheng Liu ◽

Qing-Jie Chen ◽

Ling-Peng Zeng ◽

...

Keyword(s):

Cell Proliferation ◽

Tumor Growth ◽

Radioactive Iodine ◽

Lactate Production ◽

Luciferase Reporter ◽

Current Therapy ◽

Biological Processes ◽

Reporter Assay ◽

Potential Therapeutic Target

Abstract Background During the transformation to dedifferentiated thyroid cancer (TC) types, the ability of papillary thyroid carcinomas (PTCs) to concentrate radioactive iodine might be lost, raising difficulty for the current therapy. circRNAs were proved to be implicated in the progression of various cancers. In this study, we aimed to investigate the functional role and mechanism of hsa_circ_0023990 in dedifferentiated TC. Methods The expression pattern of genes were detected using quantitative PCR or western blot assays. Cell proliferation was determined by CCK8, colony formation, EdU, and cell-cycle assays. Glycolysis was assessed using glucose uptake and lactate production assays. Luciferase reporter assay was performed to examine the interactions between miR-485-5p and hsa_circ_0023990 or FOXM1. Xenograft assay was allowed for observation of tumor growth in vivo. Results Hsa_circ_0023990 and FOXM1 were upregulated in dedifferentiated TC tissues and cell lines. The higher level of hsa_circ_0023900 could stimulate the proliferation and glycolysis of dedifferentiated TC cells via positively regulating FOXM1. Mechanistically, miR-485-5p was demonstrated to interact with hsa_circ_0023990 and FOXM1 and involved in the regulation of has_circ_0023990 and FOXM1 in TC biological processes. Conclusion Our results discovered the functional network of hsa_circ_0023990 in dedifferentiated TC development by facilitating cell proliferation and glycolysis via miR-485-5p/FOXM1 axis, implying that hsa_circ_0023990 might be a potential therapeutic target for the dedifferentiated TC treatment.

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