Epidermal Growth Factor–Independent Transformation of Ba/F3 Cells with Cancer-Derived Epidermal Growth Factor Receptor Mutants Induces Gefitinib-Sensitive Cell Cycle Progression

Background/Aims: LINC00037 has previously been reported to be up-regulated in clear cell renal cell carcinoma (ccRCC), however, the underlying mechanism remained unknown. In this study, we designed to investigate the functional role of LINC00037 in ccRCC Methods: LINC00037 knockdown and re-expressing 786-O and A498 cells were established. CCK8 assay and EdU assay were performed to evaluate the proliferation rates of ccRCC cells. Flow cytometry assay was performed to detect the cell apoptosis and cell cycle. Subcutaneous injection xenotransplantation mouse model was used to observe the role of LINC00037 in tumor growth in vivo. Mass spectrometry (MS) was performed to find the interacting partner of LINC00037 and RNA immunoprecipitation (RIP) was carried out to validate their interaction. Results: We found that knockdown of LINC00037 resulted in inhibited cell proliferation with activated apoptosis and cell cycle arrest in vitro. Over-expression of LINC00037 in LINC00037 knockdown cells restored and enhanced cell proliferation. In vivo mouse model indicated reduced tumor progression by LINC00037 depletion and promoted tumor progression by LINC00037 overexpression. LINC00037 could bind to epidermal growth factor receptor (EGFR) and increase the protein level of EGFR. Conclusion: LINC00037 could inhibit proliferation of ccRCC in an epidermal growth factor receptor-dependent way.

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Analysis of the protein glycosylation defect of a temperature-sensitive cell cycle mutant by the use of mutant cells overexpressing the human epidermal growth factor receptor after transfection of the gene

Journal of Cellular Physiology ◽

10.1002/jcp.1041330306 ◽

1987 ◽

Vol 133 (3) ◽

pp. 461-470 ◽

Cited By ~ 9

Author(s):

Jean-Jacques Feige ◽

Immo E. Scheffler

Keyword(s):

Cell Cycle ◽

Epidermal Growth Factor Receptor ◽

Growth Factor ◽

Growth Factor Receptor ◽

Protein Glycosylation ◽

Temperature Sensitive ◽

Sensitive Cell ◽

Epidermal Growth ◽

Mutant Cells ◽

Glycosylation Defect

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74 INHIBITION OF EPIDERMAL GROWTH FACTOR RECEPTOR ENHANCES RADIATION-INDUCED PERMANENT G1 ARREST SOLELY IN TUMOR CELLS WITH INTACT P53/P21 CELL CYCLE REGULATION

Radiotherapy and Oncology ◽

10.1016/s0167-8140(12)70051-8 ◽

2012 ◽

Vol 102 ◽

pp. S25-S26

Author(s):

M. Kriegs ◽

I. Brammer ◽

Y. Can ◽

T. Rieckmann ◽

M. Wang ◽

...

Keyword(s):

Cell Cycle ◽

Epidermal Growth Factor Receptor ◽

Growth Factor ◽

Epidermal Growth Factor ◽

Cell Cycle Regulation ◽

Growth Factor Receptor ◽

G1 Arrest ◽

Radiation Induced ◽

Epidermal Growth ◽

Cycle Regulation

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6-Methylsulfinylhexyl Isothiocyanate Inhibits Cell Cycle Progression in Quiescent Jb6 Cells Stimulated with Epidermal Growth Factor

Annual Research & Review in Biology ◽

10.9734/arrb/2021/v36i630386 ◽

2021 ◽

pp. 19-28

Author(s):

Takashi Hashimoto ◽

Maki Kobayashi ◽

Kazuki Kanazawa

Keyword(s):

Gene Expression ◽

Cell Cycle ◽

Growth Factor ◽

Epidermal Growth Factor ◽

Dna Synthesis ◽

Cell Cycle Progression ◽

Nuclear Antigen ◽

Cycle Progression ◽

Epidermal Growth ◽

Jb6 Cells

Objective: The effects of 6-MSITC on cell cycle progression were investigated in quiescent mouse epidermal JB6 cells. Background: 6-Methylsulfinylhexyl isothiocyanate (6-MSITC) derived from wasabi (Wasabia japonica) has been reported to prevent tumor development in vivo. Material and methods: Treatment with epidermal growth factor (EGF) to quiescent JB6 cells, which were serum-starved for 36 h, promoted cell cycle progression from the G0/G1 phase to the S phase. Effects of pretreatment with 6-MSITC on cell cycle progression were estimated by flowcytometry and real-time RT-PCR. Results: Pretreatment with 6-MSITC at 0.25-1.0 μg/ml prior to the growth stimulation with EGF significantly inhibited cell cycle progression. Pretreatment with 6-MSITC inhibited the gene expression of DNA synthesis-related proteins cyclin A2, dumbbell former 4, and proliferating cell nuclear antigen. Conclusion: These results showed that 6-MSITC inhibits cell cycle progression in quiescent cells, accompanied by the inhibition of gene expression of DNA synthesis proteins.

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