Tanshinone is the liposoluble constituent of Salia miltiorrhiza, a root used in traditional herbal medicine which is known to possess certain health benefits. Although it is known that tanshinones, including tanshinone I (T1), tanshinone IIA (T2A), and cryptotanshinone (CT), can inhibit the growth of lung cancer cells in vitro, the mechanism under which they act is still unclear. AURKA, an oncogene, encodes a serine-threonine kinase which regulates mitotic processes in mammalian cells. Here, we reported that tanshinones mediate AURKA suppression partly through up-regulating the expression of miR-32. We found that tanshinones could inhibit cell proliferation, promote apoptosis, and impede cell-cycle progression, thus performing an antineoplastic function in non-small cell lung cancer (NSCLC). Additionally, we demonstrated that tanshinones attained these effects in part by down-regulating AURKA, corroborating previous reports. Our results showed that in NSCLC, similar effects were obtained with knock-down of the AURKA gene by siRNA. We also verified that AURKA was the direct target of miR-32. Collectively, our results demonstrated that tanshinones could inhibit NSCLC by suppressing AURKA via up-regulating the expressions of miR-32 and other related miRNAs.

MicroRNAs are a class of non-coding single-stranded RNA, 20-23 nucleotide in length, which can be involved in the regulation of gene expression. Through binding with 3'-untranslated regions (3'-UTR), microRNAs can cause degradation of target mRNAs or inhibition of translation, and thus regulating the expression of genes at the post-transcriptional level. In this study, we found that miR-486-5p was significantly downregulated in non-small cell lung cancer (NSCLC) tissues and cell lines, suggesting that miR-486-5p might function as a tumor suppressor in lung cancer. Additionally, we showed that CDK4, an oncogene that plays an important role in cell cycle G1/S phase progression, was directly targeted by miR-486-5p. Furthermore, our data reveals that knockdown of CDK4 by siRNA can inhibit cell proliferation, promote apoptosis, and impede cell-cycle progression. In epigenetics, the upstream promoter of miR-486-5p was strongly regulated by methylation in NSCLC. Collectively, our results suggest that miR-486-5p could not only inhibit NSCLC by downregulating the expression of CDK4, but also be as a promising and potent therapy in the near future.

Conducting polymers are promising candidate materials in next-generation electrochromic applications due to their multicolour changes their and flexible and large-scale production capability; however, poor cycling stability and relatively low optical modulation limit widespread application. Here, a simple electrochemical deposition method is used to create a polyaniline (PANI)/Au nanorods composite electrochromic film on ITO glass as an electrode. This PANI/Au nanorods composite film has better electrochromic properties than the straight PANI film. Moreover, the electrochromic device (ECD) was successfully fabricated by PANI/Au nanorods composite film as anode and poly(3,4-ethyloxylthiophene) as the cathode. This resultant device exhibits perfect electrochromic performance, including higher optical modulation (56%), a faster response time (0.6 s for bleaching and 0.9 s for colouring) and good cycling stability (sustained 85% after 6750 cycles). Notably, the geometric structure of the film is formed by the Au nanorods coated with PANI, which not only can provide transport channel and ion storage space but also improving the conductivity. In addition, the composite structure can provide larger surface area and benefit the electrolyte ions insertion and extraction from the composite electrode film. The rational design of stacking nanocomposites on electrodes may be a useful method for fabricating high-performance ECDs.

Tanshinones which includes tanshinone I (T1), tanshinone IIA (T2A), and cryptotanshinone (CT), are the liposoluble constituent of Salia miltiorrhiza, AURKA, an oncogene, encodes a serine-threonine kinase which regulates mitotic processes in mammalian cells. Here, we reported that tanshinones mediate AURKA suppression partly through up-regulating the expression of miR-32, one of miR-25 family. We found that tanshinones could inhibit cell proliferation, promote apoptosis, and impede cell-cycle progression, thus performing an antineoplastic function in non-small cell lung cancer (NSCLC). Additionally, we demonstrated that tanshinones attained these effects in part by down-regulating AURKA, corroborating previous reports. Our results showed that in NSCLC, similar effects were obtained with knock-down of the AURKA gene by siRNA. We also verified that AURKA was the direct target of miR-32. we also found that miR-32 can promote the expression of Let-7 family, however, let-7 family down-regulates the level of miR-32. Collectively, our results demonstrated that tanshinones could inhibit NSCLC by suppressing AURKA via up-regulating the expressions of miR-25 family, let-7 family and other related miRNAs. Note: This abstract was not presented at the conference. Citation Format: zhongliang ma, bingjie zhang, yanli li. Tanshinones suppress AURKA through up-regulation of miR-32 expression in non-small cell lung cancer. [abstract]. In: Proceedings of the AACR Special Conference on Noncoding RNAs and Cancer: Mechanisms to Medicines ; 2015 Dec 4-7; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2016;76(6 Suppl):Abstract nr B14.