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Cryptotanshinone is one of the compounds extracted from the root of Salvia miltiorrhiza Bunge. Unlike other tanshinones, only a small number of studies have focused on cryptotanshinone for medical treatment. In the present study, the A549 lung cancer cell line and xenograft models of human lung tumors were used to assess the anti-cancer effect of cryptotanshinone. The effect of cryptotanshinone on human lung cancer, including growth inhibition, cell cycle arrest and apoptosis factors, were identified in vitro, and inhibition of tumor formation, improvement of body condition as well as pathological apoptotic effects were detected in vivo. These results suggested that cryptotanshinone is a potential drug for the treatment and prevention of human lung cancer.

Esophageal squamous cell carcinoma (ESCC) is the most prevalent type in esophageal cancers. Despite accumulating achievements in treatments of ESCC, patients still suffer from recurrence because of the treatment failures, one of the reasons for which is radioresistance. Therefore, it is a necessity to explore the molecular mechanism underlying ESCC radioresistance. Long intergenic noncoding RNA 473 (LINC00473) has been reported to be aberrantly expressed in several human malignancies. However, its biological function in radiosensitivity of ESCC remains to be fully understood. This study explored the role of LINC00473 in radiosensitivity of ESCC cells and whether LINC00473 acted as a competing endogenous RNA to realize its modulation on radioresistance. We found that LINC00473 was markedly upregulated in ESCC tissues and cell lines, and its expression was remarkably related to cellular response to irradiation. In addition, knockdown of LINC00473 could sensitize ESCC cells to radiation in vitro. As for the underlying mechanism, we uncovered that there was a mutual inhibition between LINC00473 and miR‐374a‐5p. Spindlin1 (SPIN1) was verified as a downstream target of miR‐374a‐5p, and LINC00473 upregulated SPIN1 expression through negatively modulating miR‐374a‐5p expression. Furthermore, we revealed that SPIN1 could aggravate the radioresistance of ESCC cells. Finally, overexpression of SPIN1 reversed the LINC00473 silencing‐enhanced radiosensitivity in ESCC cells. To sum up, we demonstrated that LINC00473 facilitated radioresistance by regulating the miR‐374a‐5p/SPIN1 axis in ESCC.

To remit capacity fading of lithium ion battery (LIB) anodes, freestanding yucca fern shaped CuO nanowires (NWs) on Cu foams are fabricated as anodes by combining facile and scalable anodization of copper foams followed by calcination. The porous and radial configuration of the hierarchical CuO NWs on the Cu foam substrate guarantees the remarkably improved electrochemical performance with durable cycle stability and excellent rate capability compared with CuO NWs on Cu foils. The reversible capacity remains 461.5 mAh/g after 100 repeated cycles at a current density of 100 mA/g, and a capacity of 150.6 mAh/g even at a high rate of 1000 mA/g. By examining the surface morphology of the cycled samples, possible performance fading route is proposed. The 3D CuO NWs network with a porous architecture simutaneously reduces the ion diffusion distances, promotes the electrolyte permeation and electronic conductivity. This novel strategy might open a new window to develop durable CuO based composite anodes for LIBs.

Nuclear factor E2 related factor 2 (Nrf2) is a transcription factor that is associated with tumor growth and resistance to radiation. The canonical Notch signaling pathway is also crucial for maintaining non-small cell lung cancer (NSCLC). Aberrant Nrf2 and Notch signaling has repeatedly been showed to facilitate metastasis of NSCLC. Here, we show that radiation induce Nrf2 and Notch1 expression in NSCLC. Knockdown of Nrf2 enhanced radiosensitivity of NSCLC and reduced epithelial-to-mesenchymal transition. Importantly, we found that knockdown of Nrf2 dramatically decreased radiation-induced NSCLC invasion and significantly increased E-cadherin, but reduced N-cadherin and matrix metalloproteinase (MMP)-2/9 expression. We found that Notch1 knockdown also upregulated E-cadherin and suppressed N-cadherin expression. Nrf2 contributes to NSCLC cell metastatic properties and this inhibition correlated with reduced Notch1 expression. These results establish that Nrf2 and Notch1 downregulation synergistically inhibit radiation-induced migratory and invasive properties of NSCLC cells.

Results: 50 mg/kg CRY significantly promoted the energy production of ATP (16.99 ± 2.38 nmol/g Pro) (Pro: Protein) by increasing the complexes activities except II (p40.05). After the treatment of CRY, the suppressed MMP was increased while superoxide anion free radical (0.57 ± 0.07/mg Pro) was inhibited markedly. Mitochondrial biogenesis-relative factors PGC-1a, NRF-1, and TFAM were also promoted. Remarkable augmentations of NO, inducible nitric oxide synthase (iNOS), and increased activity of GSH-PX (p50.05) were also detected after the treatment of CRY, while no obvious changes on the activity of nitric oxide synthase (cNOS; p40.05) were observed. Discussion and conclusion: These results suggest that CRY protects against ADR-induced mitochondrial dysfunction in cardiomyocytes. It could be an ideal potential drug of cardioprotection.

Cryptotanshinone inhibits the proliferative and colony formation abilities of human non-small cell lung cancer cells (NSCLCs). The present study reported that signal transducer and activator of transcription 3 is not the only target of cryptotanshinone during the inhibition of human NSCLCs. It was identified that cryptotanshinone upregulates the expression levels of microRNA (miR)-30d-5p, miR-126-3p, miR-133a, miR-338-3p and miR-451a, and downregulates miR-21-5p, miR-96-5p, miR-182-5p and miR-205-5p. Among these, miR-133a was the most significantly upregulated. miR-133a targets and downregulates the expression of matrix metalloproteinase (MMP)14; however, MMP15, MMP16 and MMP24 were determined to be unaffected. This process was identified to be independent of tissue inhibitor of metalloproteinases 2. Cryptotanshinone also suppresses the invasion of human NSCLCs, which may be due to the inhibited expression of MMP14. In conclusion, cryptotanshinone may serve as a potential therapeutic agent in the treatment of lung cancer.

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