Functional Study of the Human BRCA2 Tumor Suppressor

2005 ◽  
Author(s):  
Bing Xia ◽  
David M. Livingston
Keyword(s):  
Tumor Suppressor ◽  
Functional Study

MiR-485-5p as a potential biomarker and tumor suppressor in human colorectal cancer

2020 ◽  
Vol 14 (3) ◽  
pp. 239-248 ◽  
Author(s):  
Yuqin Pan ◽  
Jian Qin ◽  
Huiling Sun ◽  
Tao Xu ◽  
Shukui Wang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Suppressor ◽  
Cox Regression ◽  
Roc Curves ◽  
Functional Study ◽  
Kaplan Meier ◽  
Potential Biomarker ◽  
Polymerase Chain

Aim: To investigate the role of miR-485-5p in colorectal cancer (CRC). Methodology: The level of miR-485-5p in serum and cell lines were measured by quantitative real-time polymerase chain reaction, and analyzed the diagnostic and prognostic value. Additionally, the biological effect of miR-485-5p on CRC cells was also explored in vitro. Results: The receiver operating characteristic (ROC) curves analysis revealed that miR-485-5p was a diagnostic candidate. Kaplan-Meier analyses demonstrated that patients with low serum miR-485-5p had shorter overall survival. In addition, the result of cox regression model indicated that miR-485-5p was not an independent risk factor for progression. Functional study revealed that overexpression of miR-485-5p could inhibit CRC cell proliferation, invasion and facilitates cell apoptosis. Conclusion: Our study revealed that miR-485-5p was a tumor suppressor and it could serve as a potential prognostic biomarker in CRC.

scholarly journals Recurrent SETD2 mutation in NPM1-mutated acute myeloid leukemia

2020 ◽  
Vol 8 (1) ◽  
Author(s):  
Jiewen Sun ◽  
Wenjuan Yu ◽  
Xiang Zhang
Keyword(s):  
Acute Myeloid Leukemia ◽  
Tumor Suppressor ◽  
Cell Line ◽  
Myeloid Leukemia ◽  
Functional Study ◽  
Loss Of Function ◽  
Direct Target ◽  
And Function ◽  
Acute Myeloid

Abstract SETD2 is the only methyltransferase for H3K36me3, and our previous study has firstly demonstrated that it functioned as one tumor suppressor in hematopoiesis. Consistent with it, SETD2 mutation, which led to its loss of function, was identified in AML. However, the distribution and function of SETD2 mutation in AML remained largely unknown. Herein, we integrated SETD2-mutated AML cases from our center and literature reports, and found that NPM1 mutation was the most common concomitant genetic alteration with SETD2 mutation in AML, with its frequency even higher than MLL rearrangement and AML1-ETO. Though this result indicated the cooperation of SETD2 and NPM1 mutations in leukemogenesis, our functional study showed that SETD2 was required for the proliferation of NPM1-mutated AML cell line OCI-AML3, but not MLL-rearranged AML cell line THP-1, via maintaining its direct target NPM1 expression, which was just opposite to its role of tumor suppressor. Therefore, we speculated that SETD2 possibly had two different faces in distinct subtypes and stages of AML.

CENP-C: An oncogene or tumor suppressor gene? A possible new tumor marker

2001 ◽  
Vol 120 (5) ◽  
pp. A299-A299
Author(s):  
D KAZANOV ◽  
B STERN ◽  
W PYERIN ◽  
O BOECHER ◽  
H STRUL ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Tumor Marker ◽  
Tumor Suppressor Gene ◽  
Suppressor Gene

625: Bert-Hogg-Dubé (BHD) Tumor Suppressor Expression in Sporadic Renal Cell Carcinomas

2005 ◽  
Vol 173 (4S) ◽  
pp. 170-171 ◽  
Author(s):  
Dakun Wang ◽  
Jorge L. Yao ◽  
Edward M. Messing ◽  
Susan R. Schoen ◽  
Xiangrong He ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Renal Cell ◽  
Renal Cell Carcinomas
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