scholarly journals Synergistic Effect of Phloretin Combined With Radiotherapy on Lung Cancer

2021 ◽  
Author(s):  
Juan Tang ◽  
Youling Gong
Keyword(s):  
Lung Cancer ◽  
Synergistic Effect ◽  
Tumor Tissue ◽  
Proliferation Index ◽  
Growth Delay ◽  
Tissue Cell ◽  
Dependent Manner ◽  
Lewis Lung Cancer ◽  
Fdg Uptake ◽  
Radiotherapy Group

Abstract OBJECTIVE: The purpose of this study was to investigate the synergistic anti-tumor effects of phloretin (Ph) and radiotherapy (RT) on Lewis lung cancer (LLC), and the mechanisms involved. METHODS：The proliferative rate of Lewis cells treated with phloretin was detected by MTT assay; Clone formation experiments were used to demonstrate the synergistic effect of phloretin and radiotherapy; Mice engrafted with the LLC cells were given intraperitoneal injections of saline, phloretin with or without RT. Tumor models were established by laterally transplanting LLC cells in the right thigh of C57BL/J mice. They were randomly divided into four groups, namely saline group, phloretin group, radiotherapy group, phloretin combined with radiotherapy group. 10Gy radiotherapy was performed during the administration. PET-CT was used to detect 18F-FDG uptake in tumor tissue; immunohistochemistry was used to detect Ki67 expression in tumor tissue; cell apoptosis was detected by flow cytometry. RESULTS: Different concentrations of phloretin inhibited the proliferation of Lewis cells in a time and dose-dependent manner (P<0.05). The radiotherapy sensitization ratio (SER) of 50μg Phloretin was 1.645 in the LLC cells. The combination of Phloretin and RT increased survival compared to free Phloretin and RT (p<0.05), and prolonged tumor growth delay (TGD). Furthermore, the RT + Phloretin combination therapy significantly reduced 18F-FDG uptake, increased apoptosis and decreased the proliferation index (Ki67) in tumor cells compared to either monotherapy. CONCLUSION: phloretin combined with radiotherapy has a synergistic anti-tumor effect, possibly by promoting apoptosis, as well as inhibiting proliferation rate and glucose transport.

scholarly journals Relationship Between Non-small Cell Lung Cancer FDG Uptake at PET, Tumor Histology, and Ki-67 Proliferation Index

2008 ◽  
Vol 3 (9) ◽  
pp. 971-978 ◽  
Author(s):  
Hubert Vesselle ◽  
Alexander Salskov ◽  
Eric Turcotte ◽  
Linda Wiens ◽  
Rodney Schmidt ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Proliferation Index ◽  
Small Cell Lung ◽  
Ki 67 ◽  
Fdg Uptake ◽  
Tumor Histology

scholarly journals Antitumor Effect of Membrane-type PBLs on Non-Small Cell Lung Cancer Cell of ICR Mice

2020 ◽  
Author(s):  
Junli Cao ◽  
Peng Su ◽  
Yuefeng Zhang ◽  
Xin Wang ◽  
Xiwei Lu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Synergistic Effect ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Time Dependent ◽  
Control Group ◽  
Dependent Manner ◽  
Small Cell Lung ◽  
Icr Mice

Abstract This study aims at probing the inhibitory effect of transmembrane PBLs on non-small cell lung cancer (NSCLC) H446 cells and the potential application of PBLs on immune system of the experimental mice loaded with H446 cells. The changes of the gene expression of microRNA-25 and 223 in ICR mice with NSCLC were also investigated. Sixty ICR mice were randomly divided into experimental and control groups. The animal model was established via inoculation of NSCLC H446 cells at the hind thigh of mice. The plasmid PBLs was dissolved in saline solution and injected into the muscle of left thigh of the mice in experimental groups with different doses (0.1 mg, 0.2 mg and 0.3 mg per ICR mouse) using in situ injection method. After injection of PBLs solution, each three mice were killed at 12 h, 24 h, 36 h, and 48 h, respectively. The expression of microRNA-25 and 223 were detected by semi-quantitative reverse transcription-polymerase chain reaction. Tumor Necrosis Factor-γ (TNF-γ), Interleukelin-2 (IL-2) and Heat Shock Protein 70 (HSP70) in Bronchoalveolar Lavage Fluid (BALF) were detected by enzyme-linked immunosorbent assay. The expression of TNF-γ and IL-2 protein in lung tissue were detected by western blotting. The expression of microRNA-25 was up-regulated in the tissues and BALF with a dose- and time-dependent manner while microRNA-223 was down-regulated. The difference were statistically significant comparing the control group (P<0.05). The TNF-γ and IL-2 levels in BALF of ICR mice in experimental group were increased comparing the control group with a dose-dependent manner (P<0.05). Synergistic effect between PBLs and HSP70 was also studied. It was found that the growth of tumor was significantly suppressed after the transfection of PBLs. In the presence of PBLs, the proliferation of splenocytes and cytolysis in early phase of tumor development was significantly enhanced. Thus, such anti-tumor effect was further improved by the synergistic effect of PBLs with HSP70. The expression of microRNA-25 and 223 are associated with NSCLC in a dose- and time-dependent manner, they might be considered as potential biomarkers for early diagnosis of NSCLC.

scholarly journals Xiao-Ai-Ping, a TCM Injection, Enhances the Antigrowth Effects of Cisplatin on Lewis Lung Cancer Cells through Promoting the Infiltration and Function of CD8+T Lymphocytes

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Wanshuai Li ◽  
Yang Yang ◽  
Zijun Ouyang ◽  
Qi Zhang ◽  
Lu Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
T Cells ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Lewis Lung ◽  
Lewis Lung Cancer ◽  
Antitumor Effects ◽  
Concentration Dependent Manner ◽  
And Function

Objectives. To investigate how Xiao-Ai-Ping injection, a traditional Chinese medicine and an ancillary drug in tumor treatment, enhances the antitumor effects of cisplatin on Lewis lung cancer (LLC) cells.Methods. LLC-bearing mice were daily intraperitoneally injected with various doses of cisplatin, Xiao-Ai-Ping, or cisplatin plus Xiao-Ai-Ping, respectively. Body weight and tumor volumes were measured every three days.Results. Combination of Xiao-Ai-Ping and cisplatin yielded significantly better antigrowth and proapoptotic effects on LLC xenografts than sole drug treatment did. In addition, we found that Xiao-Ai-Ping triggered the infiltration of CD8+T cells, a group of cytotoxic T cells, to LLC xenografts. Furthermore, the mRNA levels of interferon-γ(ifn-γ), perforin-1 (prf-1), and granzyme B (gzmb) in CD8+T cells were significantly increased after combination treatment of Xiao-Ai-Ping and cisplatin.In vitrostudies showed that Xiao-Ai-Ping markedly upregulated the mRNA levels ofifn-γ,prf-1,andgzmbin CD8+T cells in a concentration-dependent manner, suggesting that Xiao-Ai-Ping augments the function of CD8+T cells.Conclusions. Xiao-Ai-Ping promotes the infiltration and function of CD8+T cells and thus enhances the antigrowth effects of cisplatin on LLC xenografts, which provides new evidence for the combination of Xiao-Ai-Ping and cisplatin in clinic in China.

scholarly journals Chidamide increases the sensitivity of non-small cell lung cancer to crizotinib by decreasing c-MET mRNA methylation

2020 ◽  
Author(s):  
Nan Ding ◽  
Abin You ◽  
Wei Tian ◽  
Liankun Gu ◽  
Dajun Deng
Keyword(s):  
Lung Cancer ◽  
Synergistic Effect ◽  
Small Cell Lung Cancer ◽  
Cell Lines ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Nsclc Cell ◽  
Dependent Manner ◽  
Free Medium ◽  
Small Cell Lung

ABSTRACTIntroductionCrizotinib is a kinase inhibitor targeting c-MET/ALK/ROS1 used as the first-line chemical for the treatment of non-small cell lung cancer (NSCLC) with ALK mutations. Although c-MET is frequently overexpressed in 35-72% of NSCLC, most NSCLCs are primarily resistant to crizotinib treatment.MethodA set of NSCLC cell lines were used to test the effect of chidamide on the crizotinib sensitivity in vitro and in vivo. Relationships between the synergistic effect of chidamide and c-MET expression and RNA methylation were systemically studied with a battery of molecular biological assays.ResultsWe found for the first time that chidamide could increase the crizotinib sensitivity of a set of ALK mutation-free NSCLC cell lines, especially those with high levels of c-MET expression. Notably, chidamide could not increase the crizotinib sensitivity of NSCLC cells cultured in serum-free medium without hepatocyte growth factor (HGF; a c-MET ligand). In contrast, the addition of HGF into the serum-/HGF-free medium could restore the synergistic effect of chidamide. Moreover, the synergistic effect of chidamide could also be abolished either by treatment with c-MET antibody or siRNA-knockdown of c-MET expression. While cells with low or no c-MET expression were primarily resistant to chidamide-crizotinib cotreatment, enforced c-MET overexpression could increase the sensitivity of these cells to chidamide-crizotinib cotreatment. Furthermore, chidamide could decrease c-MET expression by inhibiting mRNA N6-methyladenosine (m6A) modification through the downregulation of METTL3 and WTAP expression. Chidamide-crizotinib cotreatment significantly suppressed the activity of c-MET downstream molecules.Conclusionchidamide downregulated c-MET expression by decreasing its mRNA m6A methylation, subsequently increasing the crizotinib sensitivity of NSCLC cells in a c-MET-/HGF-dependent manner.GRAPHIC SUMMARY

scholarly journals Silibinin Regulates Tumor Progression and Tumorsphere Formation by Suppressing PD-L1 Expression in Non-Small Cell Lung Cancer (NSCLC) Cells

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1632
Author(s):  
Alexis Rugamba ◽  
Dong Young Kang ◽  
Nipin Sp ◽  
Eun Seong Jo ◽  
Jin-Moo Lee ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Growth Factor ◽  
Small Cell Lung Cancer ◽  
Anticancer Activity ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Molecular Signaling ◽  
Small Cell Lung

Recently, natural compounds have been used globally for cancer treatment studies. Silibinin is a natural compound extracted from Silybum marianum (milk thistle), which has been suggested as an anticancer drug through various studies. Studies on its activity in various cancers are undergoing. This study demonstrated the molecular signaling behind the anticancer activity of silibinin in non-small cell lung cancer (NSCLC). Quantitative real-time polymerase chain reaction and Western blotting analysis were performed for molecular signaling analysis. Wound healing assay, invasion assay, and in vitro angiogenesis were performed for the anticancer activity of silibinin. The results indicated that silibinin inhibited A549, H292, and H460 cell proliferation in a concentration-dependent manner, as confirmed by the induction of G0/G1 cell cycle arrest and apoptosis and the inhibition of tumor angiogenesis, migration, and invasion. This study also assessed the role of silibinin in suppressing tumorsphere formation using the tumorsphere formation assay. By binding to the epidermal growth factor receptor (EGFR), silibinin downregulated phosphorylated EGFR expression, which then inhibited its downstream targets, the JAK2/STAT5 and PI3K/AKT pathways, and thereby reduced matrix metalloproteinase, PD-L1, and vascular endothelial growth factor expression. Binding analysis demonstrated that STAT5 binds to the PD-L1 promoter region in the nucleus and silibinin inhibited the STAT5/PD-L1 complex. Altogether, silibinin could be considered as a candidate for tumor immunotherapy and cancer stem cell-targeted therapy.

scholarly journals Sevoflurane inhibits proliferation, invasion, but enhances apoptosis of lung cancer cells by Wnt/β-catenin signaling via regulating lncRNA PCAT6/ miR-326 axis

2020 ◽  
Vol 15 (1) ◽  
pp. 159-172
Author(s):  
Guoning Su ◽  
Zhibing Yan ◽  
Min Deng
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Volatile Anesthetic ◽  
Lung Cancer Cells ◽  
Luciferase Reporter ◽  
Dependent Manner ◽  
Luciferase Reporter Gene ◽  
Western Blot Assay ◽  
Gene Assay ◽  
Cancer Tissues

AbstractSevoflurane was frequently used as a volatile anesthetic in cancer surgery. However, the potential mechanism of sevoflurane on lung cancer remains largely unclear. In this study, lung cancer cell lines (H446 and H1975) were treated by various concentrations of sevoflurane. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assessment and colony formation assay were performed to detect the cell viability and proliferation, separately. Also, transwell assay or flow cytometry assay was applied as well to evaluate the invasive ability or apoptosis in lung cancer cells, respectively. Western blot assay was employed to detect the protein levels of β-catenin and Wnt5a. Moreover, quantitative real-time polymerase chain reaction (qRT-PCR) was used to examine the expression level of prostate cancer-associated transcript 6 (PCAT6) and miR-326 in lung cancer tissues and cells. The target interaction between miR-326 and PCAT6 or Wnt5a was predicted by bioinformatics analysis and verified by the dual-luciferase reporter gene assay. Sevoflurane inhibited the abilities on viability, proliferation, invasion, and activation of Wnt/β-catenin signaling, but promoted apoptosis of H446 and H1975 cells in a dose-dependent manner. The expression of PCAT6 was increased in lung cancer tissues and cells, except for that of miR-326. Besides, sevoflurane could lead to expressed limitation of PCAT6 or improvement of miR-326. This process presented a stepwise manner. Up-regulation of PCAT6 restored the suppression of sevoflurane on abilities of proliferation, invasion, rather than apoptosis, and re-activated the Wnt5a/β-catenin signaling in cells. Moreover, the putative binding sites between miR-326 and PCTA6 or Wnt5a were predicted by starBase v2.0 software online. PCAT6 suppressing effects on cells could be reversed by pre-treatment with miR-326 vector. The promotion of Wnt5a inverted effects led from miR-326 or sevoflurane. Our study indicated that sevoflurane inhibited the proliferation, and invasion, but enhanced the apoptosis in lung cancer cells by regulating the lncRNA PCAT6/miR-326/Wnt5a/β-catenin axis.

1,25(OH) 2 D 3 attenuates sleep disturbance in mouse models of Lewis lung cancer, in silico and in vivo

2021 ◽  
Author(s):  
Min Ai ◽  
Shuang‐shuang Li ◽  
Hong Chen ◽  
Xi‐ting Wang ◽  
Jiang‐nan Sun ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Sleep Disturbance ◽  
Mouse Models ◽  
In Silico ◽  
Lewis Lung ◽  
Lewis Lung Cancer
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