Chemistry, like all the natural sciences, COA of Formula: C7H7BrO, begins with the direct observation of nature— in this case, of matter.873-75-6, Name is (4-Bromophenyl)methanol, SMILES is OCC1=CC=C(Br)C=C1, belongs to bromides-buliding-blocks compound. In a document, author is Wang, Kai, introduce the new discover.
RETRACTED: LncRNA ZEB2-AS1 regulates the drug resistance of acute myeloid leukemia via the miR-142-3p/INPP4B axis (Retracted article. See vol. 11, pg. 5762, 2021)
Dysregulation of long noncoding RNAs (lncRNAs) has been reported to participate in the process of chemoresistance in multiple cancers, including acute myeloid leukemia (AML). LncRNA zinc finger E-box binding homeobox 2 antisense RNA 1 (ZEB2-AS1) has been reported to be up-regulated in AML. However, the biological role of ZEB2-AS1 remains to be determined. Quantitative real time polymerase chain reaction (qRT-PCR) was used to detect the levels of ZEB2-AS1, miR-142-3p and inositol polyphosphate-4-phosphatase type II B (INPP4B). The cell viability and apoptosis were examined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry, respectively. Western blotting was applied to analyze levels of BCL2 apoptosis regulator (Bcl-2), BCL2 associated X, apoptosis regulator (Bax), cleaved-caspase-3 and INPP4B. The interaction among ZEB2-AS1, miR-142-3p and INPP4B was verified by dual-luciferase reporter assay and RNA pull-down assay. The levels of ZEB2-AS1 and INPP4B were significantly elevated in AML and chemo-resistance tissues, as well as in THP-1 and THP-1/ADR cells. ZEB2-AS1 elevated the IC50 of ADR, and suppressed cell apoptosis of AML cells, while ZEB2-AS1 increased Bcl-2 expression and decreased the levels of Bax and cleaved-caspase-3. ZEB2-AS1 could enhance the resistance in THP-1 and THP-1/ADR cells. ZEB2-AS1 could sponge miR-142-3p, and ZEB2-AS1 reduced the promotion effect of miR-124-3p on the sensitivity of AML cells. Furthermore, IPNN4B was revealed as a target gene of miR-142-3p. More interestingly, suppression of IPNN4B by shRNA reversed the inhibitory effect of ZEB2-AS1 on the sensitivity of AML cells. LncRNA ZEB2-AS1 promoted ADR resistance of AML via regulating INP4B expression by sponging miR-142-3p, providing a novel therapeutic target for drug resistance of AML.
Note that a catalyst decreases the activation energy for both the forward and the reverse reactions and hence accelerates both the forward and the reverse reactions. you can also check out more blogs about 873-75-6. COA of Formula: C7H7BrO.