Suppression of Migration and Invasion by 4-Carbomethoxyl-10-Epigyrosanoldie E from the Cultured Soft Coral Sinularia sandensis through the MAPKs Pathway on Oral Cancer Cells.

The primary reason for cancer-related fatalities is metastasis. The compound 4-carbomethoxyl-10-epigyrosanoldie E, derived from the Sinularia sandensis soft coral species grown in cultures, exhibits properties that counteract inflammation. Moreover, it has been observed to trigger both apoptosis and autophagy within cancerous cells. This research focuses on examining the inhibitory impact of 4-carbomethoxyl-10-epigyrosanoldie E on the migration and invasion processes in Cal-27 and Ca9-22 oral cancer cell lines. To assess how this compound affects cell migration and invasion, the Boyden chamber assay was employed. Furthermore, Western blot analysis was utilized to explore the underlying molecular mechanisms. In a dose-dependent manner, 4-carbomethoxyl-10-epigyrosanoldie E notably decreased the levels of matrix metalloproteinase-2 (MMP-2) and MMP-9, along with urokinase-type plasminogen activator (uPA), in both Cal-27 and Ca9-22 cell lines. Conversely, it elevated the concentrations of tissue inhibitors of metalloproteinases-1 (TIMP-1) and TIMP-2. In addition, the treatment with this compound led to the inhibition of phosphorylation in extracellular signal-regulated kinase (ERK), p38, and c-Jun N-terminal kinase (JNK). It also curtailed the expression of several key proteins including focal adhesion kinase (FAK), protein kinase C (PKC), growth factor receptor-bound protein 2 (GRB2), Rac, Ras, Rho A, mitogen-activated protein kinase kinase kinase 3 (MEKK3), and mitogen-activated protein kinase kinase 7 (MKK7). Furthermore, the expression levels of IQ-domain GTPase-activating protein 1 (IQGAP1) and zonula occludens-1 (ZO-1) were significantly reduced by the compound. The ability of 4-carbomethoxyl-10-epigyrosanoldie E to inhibit the migration and invasion of Cal-27 and Ca9-22 oral cancer cells was observed to be dose dependent. This inhibitory effect is primarily attributed to the suppression of MMP-2 and MMP-9 expression, as well as the downregulation of the mitogen-activated protein kinase (MAPK) signaling pathway.

Calcium nanoparticles (Ca-NPs) improve drought stress tolerance in Brassica napus by modulating the photosystem II, nutrient acquisition and antioxidant performance.

Foliar-application of nano-particles enhanced the foliar nutrient status and crop growth and yield. It is hypothesized that being second messenger molecule, supplementation of Ca2+ via calcium nanoparticles (Ca-NPs) can trigger various signaling pathways of physiological processes which can lead to alleviate the adverse effects of drought stress on the growth of canola (Brassica napus L.). Nano-enabled foliar-application could be an ideal strategy for advancing agricultural productivity. The present study explored the role of calcium nanoparticles (Ca-NPs) in alleviating drought stress in hydroponic Brassica napus (B. napus) plants. The foliar applied Ca-NPs were spherically shaped with an average size of 86 nm. Foliar application of 100 mg L-1 Ca-NPs enhanced biomass of canola plants and considered as optimal dose. Ca-NPs at 100 mg L-1 has a greater favorable impact on mesophyll ultrastructure, PSI and PSII efficacy, gas exchange parameters, chlorophyll content, and mineral absorption. The Ca-NPs treatment increased NPQ and Y(NPQ) under drought condition, indicating a higher PSII protective response to stressed conditions with better heat dissipation as a photoprotective component of NPQ. Ca-NPs application also reduced oxidative stress damage as measured by a reduction in reactive oxygen species (ROS) generation in terms of hydrogen peroxide and malondialdehyde (H2O2 and MDA). Furthermore, Ca-NPs induced drought tolerance response corresponded to an increased in key antioxidative defense enzymes (SOD, POD, CAT, APX), as well as non-enzymatic components (protease, lipoxygenase, proline, total soluble protein contents, endogenous hormonal biosynthesis), and secondary metabolite expression in B. napus plants. Taken together, the results of this study offer new insights into the physiological and molecular mechanisms by which B. napus responds to Ca-NPs exposure.

Role of phytomelatonin responsive to metal stresses: An omics perspective and future scenario.

A pervasive melatonin (N-acetyl-5-methoxytryptamine) reveals a crucial role in stress tolerance and plant development. Melatonin (MT) is a unique molecule with multiple phenotypic expressions and numerous actions within the plants. It has been extensively studied in crop plants under different abiotic stresses such as drought, salinity, heat, cold, and heavy metals. Mainly, MT role is appraised as an antioxidant molecule that deals with oxidative stress by scavenging reactive oxygen species (ROS) and modulating stress related genes. It improves the contents of different antioxidant enzyme activities and thus, regulates the redox hemostasis in crop plants. In this comprehensive review, regulatory effects of melatonin in plants as melatonin biosynthesis, signaling pathway, modulation of stress related genes and physiological role of melatonin under different heavy metal stress have been reviewed in detail. Further, this review has discussed how MT regulates different genes/enzymes to mediate defense responses and overviewed the context of transcriptomics and phenomics followed by the metabolomics pathways in crop plants.

Interactive effects of biochar and mussel shell activated concoctions on immobilization of nickel and their amelioration on the growth of rapeseed in contaminated aged soil.

Mussel shell (MS) and biochar (BC) are commonly used for the remediation of metal contaminated soil. However, less research has been focused to examine the efficacy of their combinations to reduce metal toxicity in crop plants. This study was therefore conducted to investigate the effects of BC, MS and their activated concoctions on the soil properties, enzyme activities and nickel (Ni) immobilization in aged Ni contaminated soil. Moreover, the growth, photosynthetic pigments and anti-oxidative machnery of Brassica napus plants has also been investigated in order to determine amendments efficiency in reducing soil Ni toxicity for plants. The results showed that the application of Ni adversely affected soil health and trigged stress responses by inducing oxidative stress in B. napus. However, the incorporation of amendments reduced the bioavailability of Ni, and the concoctions of BC and MS showed promising results in the immobilization of Ni. Among various combinations of BC and MS, treatment with BC + MS (3:1) significantly reduced Ni uptake, decreased reactive oxygen species (ROS) and enhanced antioxidant defense of B. napus plants. Results showed that amendment's combinations stimulated the transcriptional levels of ROS scavenging enzymes and suppressed the expression level of Ni transporters. The morphological and physical characterization techniques (i.e. SEM, BET, EDS, FTIR and X-ray diffraction analyses) showed that amendment's combinations had relatively higher Ni adsorption capacity, indicating that BC and MS concoctions are efficient immobilizing agents for minimizing Ni availability, preventing oxidative toxicity and promoting growth and biomass production in rapeseed plants under metal stress conditions.

Involvement of MAPKs and NF-kappaB in tumor necrosis factor alpha-induced vascular cell adhesion molecule 1 expression in human rheumatoid arthritis synovial fibroblasts.

OBJECTIVE: To investigate the roles of MAPKs and NF-kappaB in tumor necrosis factor alpha (TNFalpha)-induced expression of vascular cell adhesion molecule 1 (VCAM-1) in human rheumatoid arthritis synovial fibroblasts (RASFs). METHODS: Human RASFs were isolated from synovial tissue obtained from patients with RA who underwent knee or hip surgery. The involvement of MAPKs and NF-kappaB in TNFalpha-induced VCAM-1 expression was investigated using pharmacologic inhibitors and transfection with short hairpin RNA (shRNA) and measured using Western blot, reverse transcriptase-polymerase chain reaction, and gene promoter assay. NF-kappaB translocation was determined by Western blot and immunofluorescence staining. The functional activity of VCAM-1 was evaluated by lymphocyte adhesion assay. RESULTS: TNFalpha-induced VCAM-1 expression, phosphorylation of p42/p44 MAPK, p38 MAPK, and JNK, and translocation of NF-kappaB were attenuated by the inhibitors of MEK-1/2 (U0126), p38 (SB202190), JNK (SP600125), and NF-kappaB (helenalin) or by transfection with their respective shRNA. TNFalpha-stimulated translocation of NF-kappaB into the nucleus and NF-kappaB promoter activity were blocked by Bay11-7082, but not by U0126, SB202190, or SP600125. VCAM-1 promoter activity was enhanced by TNFalpha in RASFs transfected with VCAM-1-Luc, and this promoter activity was inhibited by Bay11-7082, U0126, SB202190, and SP600125. Moreover, up-regulation of VCAM-1 increased the adhesion of lymphocytes to the RASF monolayer, and this adhesion was attenuated by pretreatment with helenalin, U0126, SP600125, or SB202190 prior to exposure to TNFalpha or by anti-VCAM-1 antibody before the addition of lymphocytes. CONCLUSION: In RASFs, TNFalpha-induced VCAM-1 expression is mediated through activation of the p42/p44 MAPK, p38 MAPK, JNK, and NF-kappaB pathways. These results provide new insights into the mechanisms underlying cytokine-initiated joint inflammation in RA and may inspire new targeted therapeutic approaches.