22 research outputs found
Tumor-suppressor activity of RRIG1 in breast cancer
<p>Abstract</p> <p>Background</p> <p>Retinoid receptor-induced gene-1 (RRIG1) is a novel gene that has been lost in several types of human cancers. The aim of this study was to determine whether RRIG1 plays a role in breast cancer, such as in the suppression of breast cancer cell growth and invasion.</p> <p>Methods</p> <p>Immunohistochemistry was used to detect RRIG1 expression in breast tissue specimens. Gene transfection was used to restore or knock down RRIG1 expression in breast cancer cell lines for analysis of cell viability, colony formation, and migration/invasion potential. Reverse-transcription polymerase chain reaction and western blot assays were used to detect the changes in gene expression. The RhoA activation assay was used to assess RRIG1-induced inhibition of RhoA activity.</p> <p>Results</p> <p>The immunohistochemical data showed that <it>RRIG1 </it>expression was reduced in breast cancer tissues compared with normal and atypical hyperplastic breast tissues. <it>RRIG1 </it>expression was inversely correlated with lymph node metastasis of breast cancer but was not associated with the status of hormone receptors, such as estrogen receptor, progesterone receptor, or HER2. Furthermore, restoration of <it>RRIG1 </it>expression inhibited proliferation, colony formation, migration, and invasion of breast cancer cells. Expression of RRIG1 also reduced phosphorylated Erk1/2 and Akt levels; c-Jun, MMP9, and Akt expressions; and RhoA activity. In contrast, knockdown of RRIG1 expression promoted breast cancer cell proliferation, colony formation, migration, and invasion potential.</p> <p>Conclusion</p> <p>The data from the current study indicated that <it>RRIG1 </it>expression was reduced or lost in breast cancer and that restoration of RRIG1 expression suppressed breast cancer cell growth and invasion capacity. Future studies will determine the underlying molecular mechanisms and define RRIG1 as a tumor-suppressor gene in breast cancer.</p
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Insulin growth factor 2 mRNA binding protein 1 (IGF2BP1) regulates translation of the multidrug resistance protein 2 (MRP2) by binding to its 5â˛âuntranslated region (5â˛UTR)
MRP2 is a member of the ATP binding cassette superfamily (ABC) of efflux transporters and mediates the ATPâdependent efflux of glucuronide and glutathione conjugates from liver, kidney and intestinal cells. The MRP2 5â˛UTR was investigated for its regulation of downstream gene expression. Both transient gene expression in HepG2 cells and in vitro translation assays of MRP2 5â˛UTRâluciferase constructs showed that a 35 nt RNA motif in the MRP2 5â˛UTR stimulates downstream open reading frame (ORF) translation. One, 2, 3 and 5 copies of the 35 nt motif were inserted between renilla and firefly luciferase ORFs in bicistronic constructs and transfected into HepG2 cells, where analysis of gene expression showed that the 35 nt motif enhanced translation of the 3Ⲡcistron without affecting its mRNA expression. In vitro translation assays of the bicistronic transcripts showed that the 35 nt motif increased translation of the 3Ⲡcistron, consistent with potential Internal Ribosome Entry Site (IRES) activity of the 35 nt RNA motif. Using RNA EMSA, affinity purification and Mass Spectrometry, IGF2BP1 was identified as a protein that bound to the 35 nt RNA motif, while overâexpression of IGF2BP1 in HepG2 cells increased MRP2 translation. Thus, IGF2BP1 stimulates capâdependent and capâindependent translation initiation through binding to the MRP2 5â˛UTR 35 nt motif
Overall-effective measures for sustainable water resources management in the coastal areas of Shandong Province, China
Application of grey relational analysis and extreme learning machine method for predicting silicon content of molten iron in blast furnace
RESEARCH Open Access
cooperatively mediates GSK3-dependent Mcl-1 degradation induced by the Akt inhibitor API-1, resulting in apoptosi