scholarly journals The Effect of Dark Septate Endophytic Fungi on Mahonia oiwakensis

Plants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1723
Author(s):  
Lei-Chen Lin ◽  
Yin-Ling Tan ◽  
Wan-Rou Lin ◽  
Kuo-Lung Ku ◽  
Shang-Tse Ho

This is the first study to discuss the effects of dark septate endophytes (DSE) on the growth promotion and berberine concentration in Mahonia oiwakensis, whose extract (MOE) has been suggested to have potential therapeutic effects against human lung cancer. First, as per phylogenetic analysis, the strains were divided into four groups: CkDB2, CkDB5, MoAL2 and MoAL5. All of these were DSEs, which could form microsclerotia in M. oiwakensis. The growth response experiment revealed that inoculation of the plant with MoAL5 and CkDB5 promoted an increase in the total fresh weight of the seedlings. Chemical composition analysis showed that seedlings inoculated with CkDB5 had the highest berberine concentration. These results showed that some DSEs have the ability to promote growth and induce phytochemical responses in the host plant.

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Meghan M. Cromie ◽  
Weimin Gao

Our previous studies have shown Leptomycin B (LMB) is a promising antilung cancer drug. Epigallocatechin-3-gallate (EGCG) has antitumor properties but a debatable clinical application. The objective of this study is to evaluate the combination therapeutic effect of LMB and EGCG and its molecular mechanisms in human lung cancer A549 cells. Increased cytotoxicity was observed in LMB+EGCG-treated cells compared to LMB-treated cells. Elevated ROS was maximized 2 h after treatment, and LMB+EGCG-treated cells had higher ROS levels compared to LMB. N-Acetyl-L-cysteine (NAC) studies confirmed the oxidative role of LMB and/or EGCG treatment. In comparison to the control, CYP3A4, SOD, GPX1, and p21 mRNA expression levels were increased 7.1-, 2.0-, 4.6-, and 13.1-fold in LMB-treated cells, respectively, while survivin was decreased 42.6-fold. Additionally, these increases of CYP3A4, SOD, and GPX1 were significantly reduced, while p21 was significantly increased in LMB+EGCG-treated cells compared to LMB-treated cells. The qRT-PCR results for p21 and survivin were further confirmed by Western blot. Our study first shows that LMB produces ROS and is possibly metabolized by CYP3A4, GPX1, and SOD in A549 cells, and combination treatment of LMB and EGCG augments LMB-induced cytotoxicity through enhanced ROS production and the modulation of drug metabolism and p21/survivin pathways.


BMC Cancer ◽  
2007 ◽  
Vol 7 (1) ◽  
Author(s):  
Xulong Zhang ◽  
Jian Zhang ◽  
Lihua Wang ◽  
Haiming Wei ◽  
Zhigang Tian

Pharmacology ◽  
2020 ◽  
pp. 1-15
Author(s):  
Jyh-Cheng Chen ◽  
Jen-Chung Ko ◽  
Yong-Cing Taso ◽  
Hsiang-Hung Cheng ◽  
Tzu-Ying Chen ◽  
...  

<b><i>Introduction:</i></b> Xeroderma pigmentosum complementation group C (XPC) protein is an important DNA damage recognition factor involved in nucleotide excision repair and regulation of non-small-cell lung cancer (NSCLC) cell proliferation and viability. 17-Allylamino-17-demethoxygeldanamycin (17-AAG) blocks ATP binding to heat shock protein 90 (Hsp90), resulting in destabilization of Hsp90-client protein complexes. Vascular endothelial growth factor (VEGF) is a potent angiogenic growth factor expressed by many types of tumors. Bevacizumab (Avastin) is a humanized monoclonal antibody against human VEGF used as an antiangiogenesis agent in the therapy of many cancers, proving successful in increasing objective tumor response rate and prolonging overall survival in NSCLC patients. <b><i>Methods:</i></b> After the bevacizumab and/or 17-AAG treatment, the expressions of XPC mRNA were determined by quantitative real-time PCR analysis. Protein levels of XPC and phospho-AKT were determined by Western blot analysis. We used specific XPC small interfering RNA and PI3K inhibitor (LY294002) to examine the role of the AKT-XPC signal in regulating the chemosensitivity of bevacizumab and 17-AAG. Cell viability was assessed by the MTS assay and trypan blue exclusion assay. <b><i>Results:</i></b> In this study, bevacizumab decreased XPC expression in human lung squamous cell carcinoma H520 and H1703 cells via AKT inactivation. Enhancement of AKT activity by transfection with constitutively active AKT vectors increased XPC expression and cell survival after treatment with bevacizumab. In addition, 17-AAG synergistically enhanced bevacizumab-induced cytotoxicity and cell growth inhibition in H520 and H1703 cells, associated with downregulation of XPC expression and inactivation of AKT. <b><i>Discussion/Conclusion:</i></b> Together, these results may provide a rationale to combine bevacizumab with Hsp90 inhibitors in future to enhance therapeutic effects for lung cancer.


Author(s):  
Benjamin Gaston ◽  
Nadzeya Marozkina

Author(s):  
Geyu Liang ◽  
Xikai Wang ◽  
Yanqiu Zhang ◽  
Yanyun Fu ◽  
Lihong Yin ◽  
...  

2017 ◽  
Vol 5 (1) ◽  
Author(s):  
Lingyan Wang ◽  
Jiayun Hou ◽  
Minghuan Zheng ◽  
Lin Shi

Actinidia Chinensis Planch roots (acRoots) are used to treat many cancers, although the anti-tumor mechanism by which acRoots inhibit cancer cell growth remains unclear. The present study aims at investigating inhibitory effects of acRoots on human lung cancer cells and potential mechanisms. Our data demonstrate that the inhibitory effects of acRoots on lung cancer cells depend on genetic backgrounds and phenotypes of cells. We furthermore found the expression of metabolism-associated gene profiles varied between acRoots-hypersensitive (H460) or hyposensitive lung cancer cells (H1299) after screening lung cancer cells with different genetic backgrounds. We selected retinoic acid receptor beta (RARB) as the core target within metabolism-associated core gene networks and evaluated RARB changes and roles in cells treated with acRoots at different concentrations and timeframes. Hypersensitive cancer cells with the deletion of RARB expression did not response to the treatment with acRoots, while RARB deletion did not change effects of acRoots on hyposensitive cells. Thus, it seems that RARB as the core target within metabolism-associated networks plays important roles in the regulation of lung cancer cell sensitivity to acRoots.


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