Past studies have shown that amplified insulin-like growth factor 1 (IGF1)/IGF1 receptor (IGF1-R) signalling has an important role in colorectal cancer (CRC) development, progression and resistance to treatment. In this report, we demonstrate that downregulation of microRNA-497 (miR-497) as a result of DNA copy number reduction is involved in upregulation of IGF1-R in CRC cells. MiR-497 and miR-195 of the miR-15/16/195/424/497 family that share the same 3′ untranslated region (3′UTR) binding seed sequence and are predicted to target IGF1-R were concurrently downregulated in the majority of CRC tissues relative to paired adjacent normal mucosa. However, only overexpression of miR-497 led to suppression of the IGF1-R 3′UTR activity and downregulation of the endogenous IGF1-R protein in CRC cells. This was associated with inhibition of cell survival, proliferation and invasion, and increased sensitivity to apoptosis induced by various stimuli including the chemotherapeutic drugs cisplatin and 5-fluorouracil, and the death ligand tumour necrosis factor-related apoptosis-inducing ligand. The biological effect of miR-497 on CRC cells was largely mediated by inhibition of phosphatidylinositol 3-kinase/Akt signalling, as overexpression of an active form of Akt reversed its impact on cell survival and proliferation, recapitulating the effect of overexpression of IGF1-R. Downregulation of miR-497 and miR-195 appeared to associate with copy number loss of a segment of chromosome 17p13.1, where these miRs are located at proximity. Similarly to miR-195, the members of the same miR family, miR-424 that was upregulated, and miR-15a, miR-15b and miR-16 that were unaltered in expression in CRC tissues compared with paired adjacent normal mucosa, did not appear to have a role in regulating the expression of IGF1-R. Taken together, these results identify downregulation of miR-497 as an important mechanism of upregulation of IGF1-R in CRC cells that contributes to malignancy of CRC.
We demonstrate a low-cost and effective method to fabricate hexagonally patterned, vertically aligned ZnO nanorod arrays. Selective wet-etching is used to develop the catalyzing gold particle hexagonal pattern with the aid of a polystyrene microsphere self-assembled monolayer. The gold particles have tunable sizes independent of the polystyrene microsphere's diameter and are inherently round in shape. Each ZnO rod is grown individually from a catalyzing site via catalyst-initiated epitaxy, and the original hexagonal periodicity is well-preserved. The rods have flat ends, and the diameters of the rods can be controlled well by the amount of source materials. This method provides a promising way to create ZnO one-dimensional nanostructures for applications as two-dimensional photonic crystal, sensor arrays, nanolaser arrays, and optoelectronic devices.
Long, straight gallium nitride nanowires, such as those shown in the Figure, are reported to have been grown directly on substrates, without templates, from the reaction of ammonium with metal gallium. Nanoparticle catalysts and directed flow of the carrier gas are shown to be the main factors leading to the quasi‐1D growth. GaN nanowires can be used to improve the performance of certain optoelectronic devices.
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