Comparative Transcriptome Analysis Provides Insights into the Effect of Epicuticular Wax Accumulation on Salt Stress in Coconuts.

The coconut is an important tropical economical crop and exhibits high tolerance to various types of salinity stress. However, little is known about the molecular mechanism underlying its salt tolerance. In this study, RNA-Seq was applied to examine the different genes expressed in four coconut varieties when exposed to a salt environment, resulting in the generation of data for 48 transcriptomes. Comparative transcriptome analysis showed that some genes involved in cutin and wax biosynthesis were significantly upregulated in salt treatment compared to the control, including CYP86A4, HTH, CER1, CER2, CER3, DCR, GPAT4, LTP3, LTP4, and LTP5. In particular, the expression of CER2 was induced more than sixfold, with an RPKM value of up to 205 ten days after salt treatment in Hainan Tall coconut, demonstrating superior capacity in salt tolerance compared to dwarf coconut varieties. However, for yellow dwarf and red dwarf coconut varieties, the expression level of the CER2 gene was low at four different time points after exposure to salt treatment, suggesting that this gene may contribute to the divergence in salt tolerance between tall and dwarf coconut varieties. Cytological evidence showed a higher abundance of cuticle accumulation in tall coconut and severe damage to cuticular wax in dwarf coconut.

WSD-0922, a novel brain-penetrant inhibitor of epidermal growth factor receptor, promotes survival in glioblastoma mouse models.

Background: Although the epidermal growth factor receptor (EGFR) is a frequent oncogenic driver in glioblastoma (GBM), efforts to therapeutically target this protein have been largely unsuccessful. The present preclinical study evaluated the novel EGFR inhibitor WSD-0922. Methods: We employed flank and orthotopic patient-derived xenograft models to characterize WSD-0922 and compare its efficacy to erlotinib, a potent EGFR inhibitor that failed to provide benefit for GBM patients. We performed long-term survival studies and collected short-term tumor, plasma, and whole-brain samples from mice treated with each drug. We utilized mass spectrometry to measure drug concentrations and spatial distribution and to assess the impact of each drug on receptor activity and cellular signaling networks. Results: WSD-0922 inhibited EGFR signaling as effectively as erlotinib in in vitro and in vivo models. While WSD-0922 was more CNS penetrant than erlotinib in terms of total concentration, comparable concentrations of both drugs were measured at the tumor site in orthotopic models, and the concentration of free WSD-0922 in the brain was significantly less than the concentration of free erlotinib. WSD-0922 treatment provided a clear survival advantage compared to erlotinib in the GBM39 model, with marked suppression of tumor growth and most mice surviving until the end of the study. WSD-0922 treatment preferentially inhibited phosphorylation of several proteins, including those associated with EGFR inhibitor resistance and cell metabolism. Conclusions: WSD-0922 is a highly potent inhibitor of EGFR in GBM, and warrants further evaluation in clinical studies.

Long noncoding RNA KCNQ1 opposite strand/antisense transcript 1 promotes osteosarcoma progression through miR-154-3p/KLF12.

OBJECTIVE: Osteosarcoma (OS) is a common bone cancer that usually influences children. Metastasis and recurrence are the main reasons for the poor prognosis. In this study, we investigated the functions and mechanisms of KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) in OS. METHODS: Cell viability and proliferation were detected using the CCK-8 assay and the 5-Ethynyl-2'-deoxyuridine (EdU) assay. Wound-healing assays, transwell assay and flow cytometry were used to identify cell migration, invasion, and apoptosis, respectively. The relationship among KCNQ1OT1, miR-154-3p, and KLF12 was verified by luciferase reporter assay and restricting protein immunoprecipitation (RIP) assay. Xenograft models were established to confirm the function of KCNQ1OT1 in vivo. RESULTS: The expression of KCNQ1OT1 was higher in OS than in non-tumor tissues and cells. Knockdown of KCNQ1OT1 could reduce OS cell proliferation, migration, and invasion and promoted cell death. Mechanistically, KCNQ1OT1 contributed to OS formation by acting as a competitive endogenous RNA (ceRNA) and influencing miR-154-3p expression. Furthermore, we confirmed that miR-154-3p affected KLF12 expression through binding the 3'UTR region. Finally, rescue experiments determined that KCNQ1OT1 exerted major roles in OS through the miR-154-3p/KLF12 axis. CONCLUSION: In conclusion, our research explains the mechanism of KCNQ1OT1 in OS progression, which could serve as a new therapeutic target.

Cloning Coconut via Somatic Embryogenesis: A Review of the Current Status and Future Prospects.

Coconut [Cocos nucifera L.] is often called "the tree of life" because of its many uses in the food, beverage, medicinal, and cosmetic industries. Currently, more than 50% of the palms grown throughout the world are senile and need to be replanted immediately to ensure production levels meet the present and increasing demand for coconut products. Mass replanting will not be possible using traditional propagation methods from seed. Recent studies have indicated that in vitro cloning via somatic embryogenesis is the most promising alternative for the large-scale production of new coconut palms. This paper provides a review on the status and prospects for the application of somatic embryogenesis to mass clonal propagation of coconut.