scholarly journals Human Biofield Therapy and the Growth of Mouse Lung Carcinoma

2019 ◽  
Vol 18 ◽  
pp. 153473541984079 ◽  
Author(s):  
Peiying Yang ◽  
Yan Jiang ◽  
Patrea R. Rhea ◽  
Tara L. Conway ◽  
Dongmei Chen ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Cancer Cells ◽  
Lung Carcinoma ◽  
Immune Cell ◽  
Lung Tumor ◽  
Reversed Phase ◽  
Mouse Lung ◽  
Control Group ◽  
Experimental Exposure ◽  
Immune Cell Population

Biofield therapies have gained popularity and are being explored as possible treatments for cancer. In some cases, devices have been developed that mimic the electromagnetic fields that are emitted from people delivering biofield therapies. However, there is limited research examining if humans could potentially inhibit the proliferation of cancer cells and suppress tumor growth through modification of inflammation and the immune system. We found that human NSCLC A549 lung cancer cells exposed to Sean L. Harribance, a purported healer, showed reduced viability and downregulation of pAkt. We further observed that the experimental exposure slowed growth of mouse Lewis lung carcinoma evidenced by significantly smaller tumor volume in the experimental mice (274.3 ± 188.9 mm3) than that of control mice (740.5 ± 460.2 mm3; P < .05). Exposure to the experimental condition markedly reduced tumoral expression of pS6, a cytosolic marker of cell proliferation, by 45% compared with that of the control group. Results of reversed phase proteomic array suggested that the experimental exposure downregulated the PD-L1 expression in the tumor tissues. Similarly, the serum levels of cytokines, especially MCP-1, were significantly reduced in the experimental group ( P < .05). Furthermore, TILs profiling showed that CD8+/CD4− immune cell population was increased by almost 2-fold in the experimental condition whereas the number of intratumoral CD25+/CD4+ (T-reg cells) and CD68+ macrophages were 84% and 33%, respectively, lower than that of the control group. Together, these findings suggest that exposure to purported biofields from a human is capable of suppressing tumor growth, which might be in part mediated through modification of the tumor microenvironment, immune function, and anti-inflammatory activity in our mouse lung tumor model.

Recombinant adeno-associated virus 9-mediated expression of Kallistatin suppresses lung tumor growth in mice

2020 ◽  
Vol 20 ◽  
Author(s):  
Weihong Qu ◽  
Jianguo Zhao ◽  
Yaqing Wu ◽  
Ruian Xu ◽  
Shaowu Liu
Keyword(s):  
Lung Cancer ◽  
Gene Therapy ◽  
Tumor Growth ◽  
Lung Tumor ◽  
Control Group ◽  
High Dose ◽  
Blank Control Group ◽  
Adeno Associated Virus ◽  
Tumor Tissues ◽  
Subcutaneous Xenograft

Background:: Lung cancer remains the most common cause of cancer-related deaths in China and worldwide. Traditional surgery and chemotherapy do not offer an effective cure although gene therapy may be a promising future alter-native. Kallistatin (Kal) is an endogenous inhibitor of angiogenesis and tumorigenesis. Recombinant adeno-associated virus (rAAV) is considered the most promising vector for gene therapy of many diseases due to persistent and long-term transgen-ic expression. Objective:: The aim of this study was to investigate whether rAAV9-Kal inhibited NCI-H446 subcutaneous xenograft tumor growth in mice. Method:: The subcutaneous xenograft mode were induced by subcutaneous injection of 2×106 H446 cells into the dorsal skin of BALB/c nude mice. The mice were administered with ssrAAV9-Kal (single-stranded rAAV9) or dsrAAV9-Kal (double-stranded rAAV9）by intraperitoneal injection (I.P.). Tumor microvessel density (MVD) was examined by anti-CD34 stain-ing to evaluate tumor angiogenesis. Results:: Compared with the PBS (blank control) group, tumor growth in the high-dose ssrAAV9-Kal group was inhibited by 40% by day 49, and the MVD of tumor tissues was significantly decreased. Conclusion:: The results indicate that this therapeutic strategy is a promising approach for clinical cancer therapy and impli-cate rAAV9-Kal as a candidate for gene therapy of lung cancer.

scholarly journals The Pro-Survival Oct4/Stat1/Mcl-1 Axis Is Associated with Poor Prognosis in Lung Adenocarcinoma Patients

Cells ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2642
Author(s):  
Yu-Chu Su ◽  
Yi-Cheng Chen ◽  
Yau-Lin Tseng ◽  
Gia-Shing Shieh ◽  
Pensee Wu ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Lung Adenocarcinoma ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Poor Prognosis ◽  
Lung Tumor ◽  
Embryonic Stem ◽  
Physiological Role ◽  
Stem Cell Marker ◽  
Apoptosis Pathway

The embryonic stem cell marker Oct4 is expressed in several human cancers and is positively correlated with a poor outcome in cancer patients. However, its physiological role in cancer progression remains poorly understood. Tumor cells block apoptosis to escape cell death so that they can proliferate indefinitely, leading to ineffective therapy for cancer patients. In this study, we investigated whether Oct4 regulates the apoptosis pathway and contributes to poor prognosis in patients with lung adenocarcinoma. Our results revealed that Oct4 expression is correlated with Stat1 expression in lung adenocarcinoma patients and Oct4 is directly bound to the Stat1 promoter to transactivate Stat1 in lung adenocarcinoma cells. Expression of the Stat1 downstream gene Mcl-1 increased in Oct4-overexpressing cancer cells, while Stat1 knockdown in Oct4-overexpressing cancer cells sensitized them to cisplatin-induced apoptosis. Furthermore, Oct4 promoted Stat1 expression and tumor growth, whereas silencing of Stat1 reduced Oct4-induced tumor growth in human lung tumor xenograft models. Taken together, we demonstrate that Oct4 is a pro-survival factor by inducing Stat1 expression and that the Oct4/Stat1/Mcl-1 axis may be a potential therapeutic target for lung adenocarcinoma.

Paracrine Suppression of VEGF Secretion by Erythropoietin Inhibits Tumor Growth.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3909-3909
Author(s):  
Carroll R. Smith ◽  
Kenneth J. Salleng ◽  
Vaia Y. Sigounas ◽  
Adam Asch ◽  
George Sigounas
Keyword(s):  
Tumor Growth ◽  
Lung Carcinoma ◽  
Lewis Lung Carcinoma ◽  
Lung Metastases ◽  
Control Group ◽  
Lewis Lung ◽  
Average Volume ◽  
Primary Tumors ◽  
Significant Difference

Abstract Several studies have reported that erythropoietin (Epo) is a pleiotropic cytokine with biological properties in addition to its primary function in regulating maturation, growth and survival along the erythroid lineage. Recently, a number of investigators have reported that various neoplastic tissues and human cancer cell lines express Epo and the Epo receptor (EpoR), raising suspicion for the presence of an autocrine-paracrine Epo-EpoR system. It has been shown that inhibition of vascular endothelial growth factor (VEGF) results in an increase of Epo secretion and increased hematocrit in vivo. In this study, we used an in vivo Lewis lung carcinoma model to examine a converse Epo effect on VEGF production and metastasis. Lewis lung carcinoma (LLC) cells were injected subcutaneously into C57BL mice. The plasma levels of VEGF, the tumor vessel formation, the size of the primary tumors and the extent of lung metastatic disease were determined. In addition, intravenously injected LLC cells seeded in the lungs were assessed. Tumor-bearing animals treated with Epo had 23.6% less VEGF in the plasma compared to saline treated mice (p&lt;0.04). There was no correlation between VEGF concentration and hemoglobin levels in either group of animals. Tumor sections indicated that the number of blood vessels was higher (10.7% for inner and 23.8% for outer, respectively) in tumors obtained from animals treated with saline compared to Epo-treated mice (p&gt;0.05). Using non-parametric analysis, we found that there was a statistically significant difference in tumor growth between saline-treated and Epo-treated animals (p&lt;0.05). However, the number of lung metastases derived from primary tumors was similar in both groups. In assessing size of the metastatic tumors, we found that the average volume of lung nodules was 24.2% higher in saline-injected animals compared to Epo-treated mice. The number of tumors seeded in the lungs following intravenous injection of LLC cells was similar in animals treated with a high dosage of Epo, low dosage of Epo or saline. In addition, the average volume of the nodules was reduced by 42% in animals treated with high and low concentrations of Epo compared to the control group (p = 0.03). In conclusion, Epo exerts a paracrine suppressive effect on VEGF secretion resulting in slower tumor growth in this model.

scholarly journals Leveling Up the Controversial Role of Neutrophils in Cancer: When the Complexity Becomes Entangled

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2486
Author(s):  
Ronit Vogt Sionov
Keyword(s):  
Tumor Growth ◽  
Tumor Cell ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Immune Cell ◽  
Neutrophil Function ◽  
The Body ◽  
Cathepsin G ◽  
Metastatic Sites

Neutrophils are the most abundant immune cell in the circulation of human and act as gatekeepers to discard foreign elements that have entered the body. They are essential in initiating immune responses for eliminating invaders, such as microorganisms and alien particles, as well as to act as immune surveyors of cancer cells, especially during the initial stages of carcinogenesis and for eliminating single metastatic cells in the circulation and in the premetastatic organs. Since neutrophils can secrete a whole range of factors stored in their many granules as well as produce reactive oxygen and nitrogen species upon stimulation, neutrophils may directly or indirectly affect carcinogenesis in both the positive and negative directions. An intricate crosstalk between tumor cells, neutrophils, other immune cells and stromal cells in the microenvironment modulates neutrophil function resulting in both anti- and pro-tumor activities. Both the anti-tumor and pro-tumor activities require chemoattraction towards the tumor cells, neutrophil activation and ROS production. Divergence is seen in other neutrophil properties, including differential secretory repertoire and membrane receptor display. Many of the direct effects of neutrophils on tumor growth and metastases are dependent on tight neutrophil–tumor cell interactions. Among them, the neutrophil Mac-1 interaction with tumor ICAM-1 and the neutrophil L-selectin interaction with tumor-cell sialomucins were found to be involved in the neutrophil-mediated capturing of circulating tumor cells resulting in increased metastatic seeding. On the other hand, the anti-tumor function of neutrophils was found to rely on the interaction between tumor-surface-expressed receptor for advanced glycation end products (RAGE) and Cathepsin G expressed on the neutrophil surface. Intriguingly, these two molecules are also involved in the promotion of tumor growth and metastases. RAGE is upregulated during early inflammation-induced carcinogenesis and was found to be important for sustaining tumor growth and homing at metastatic sites. Cathepsin G was found to be essential for neutrophil-supported lung colonization of cancer cells. These data level up the complexity of the dual role of neutrophils in cancer.

scholarly journals Monocarboxylate Transporter-2 Expression Restricts Tumor Growth in a Murine Model of Lung Cancer: A Multi-Omic Analysis

2021 ◽  
Vol 22 (19) ◽  
pp. 10616
Author(s):  
Abdelnaby Khalyfa ◽  
Zhuanhong Qiao ◽  
Murugesan Raju ◽  
Chi-Ren Shyu ◽  
Lyndon Coghill ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Growth ◽  
Lung Carcinoma ◽  
Cell Activation ◽  
Monocarboxylate Transporter ◽  
Mouse Lung ◽  
Host Immune System ◽  
B Cell Activation ◽  
Fecal Microbiome ◽  
Local Invasion

Monocarboxylate transporter 2 (MCT2) is a major high-affinity pyruvate transporter encoded by the SLC16A7 gene, and is associated with glucose metabolism and cancer. Changes in the gut microbiota and host immune system are associated with many diseases, including cancer. Using conditionally expressed MCT2 in mice and the TC1 lung carcinoma model, we examined the effects of MCT2 on lung cancer tumor growth and local invasion, while also evaluating potential effects on fecal microbiome, plasma metabolome, and bulk RNA-sequencing of tumor macrophages. Conditional MCT2 mice were generated in our laboratory using MCT2loxP mouse intercrossed with mCre-Tg mouse to generate MCT2loxP/loxP; Cre+ mouse (MCT2 KO). Male MCT2 KO mice (8 weeks old) were treated with tamoxifen (0.18 mg/g BW) KO or vehicle (CO), and then injected with mouse lung carcinoma TC1 cells (10 × 105/mouse) in the left flank. Body weight, tumor size and weight, and local tumor invasion were assessed. Fecal DNA samples were extracted using PowerFecal kits and bacterial 16S rRNA amplicons were also performed. Fecal and plasma samples were used for GC−MS Polar, as well as non-targeted UHPLC-MS/MS, and tumor-associated macrophages (TAMs) were subjected to bulk RNAseq. Tamoxifen-treated MCT2 KO mice showed significantly higher tumor weight and size, as well as evidence of local invasion beyond the capsule compared with the controls. PCoA and hierarchical clustering analyses of the fecal and plasma metabolomics, as well as microbiota, revealed a distinct separation between the two groups. KO TAMs showed distinct metabolic pathways including the Acetyl-coA metabolic process, activation of immune response, b-cell activation and differentiation, cAMP-mediated signaling, glucose and glutamate processes, and T-cell differentiation and response to oxidative stress. Multi-Omic approaches reveal a substantial role for MCT2 in the host response to TC1 lung carcinoma that may involve alterations in the gut and systemic metabolome, along with TAM-related metabolic pathway. These findings provide initial opportunities for potential delineation of oncometabolic immunomodulatory therapeutic approaches.

Bronchogenic and alveologenic tumors in mice induced by N-nitrosopiperidineThis paper is one of a selection of papers published in this special issue entitled “Second International Symposium on Recent Advances in Basic, Clinical, and Social Medicine” and has undergone the Journal's usual peer review process.

2010 ◽  
Vol 88 (4) ◽  
pp. 775-782 ◽  
Author(s):  
Xiao-Yuan Xie ◽  
Jian Shen ◽  
Li-Yan Xu ◽  
En-Min Li ◽  
Zhong-Ying Shen
Keyword(s):  
Lung Tumor ◽  
Morphological Changes ◽  
Peer Review Process ◽  
Tumor Formation ◽  
Mouse Lung ◽  
Control Group ◽  
Alveolar Type ◽  
Mrna Levels ◽  
Pulmonary Cancer ◽  
Experimental Group

The aim of this study was to explore the histogenesis and carcinogenesis of pulmonary cancer induced by N-nitrosopiperidine (NPIP) in mice. NPIP is a form of N-nitrosamine found in tobacco smoke, which has been shown to be a genotoxic chemical as well as a mutagenic compound for inducing chromosome aberrations and severe clastogenicity. In this study, 80 BALB/C strain mice were injected with 0.2 mmol/kg NPIP intraperitoneally for 8 weeks, and experiments were conducted for a further 16 weeks. For the control group, 40 mice were injected with an equal volume of 0.9% NaCl. Pulmonary tissues and tumors in the NPIP-treated group were examined by light microscopy and transmission electron microscopy and compared with the control group at 4-week intervals. The mRNA levels of p53 (mutant), bcl-2, c-myc, ras, and subunits of telomerase — telomerase reverse transcriptase (TERT) and an RNA component, TR — were assayed by mPCR or RT–PCR. Twenty-two mice in the experimental group were found to develop pulmonary tumors, but none in the control group. All tumors found in the experimental group originated from alveolar type II epithelial cells. In addition, 6 of the 22 mice also developed tumors of bronchogenic origin. The expression of p53, bcl-2, c-myc, ras, and the subunits of telomerase were found to increase in all pulmonary tissues and tumors formed thereafter upon NPIP treatment. In summary, NPIP-induced mouse lung tumors exhibited morphological changes during carcinogenesis, which may be the consequence of overexpression of some genes associated with the development of carcinoma and changes in subunits of telomerase. This mouse model of lung tumor formation may be a useful tool to delineate the histogenesis and carcinogenesis of human pulmonary cancer.

HSP70 Promotes Heat Tolerance Effect of Lung Cancer Cells Through Mediating SUMOylation of HIF-1α

2020 ◽  
Vol 10 (8) ◽  
pp. 1077-1084
Author(s):  
Jun Wan ◽  
Min Zhou ◽  
Xiean Ling ◽  
Guanggui Ding ◽  
Jian Wang
Keyword(s):  
Lung Cancer ◽  
T Cells ◽  
Cancer Cells ◽  
Heat Tolerance ◽  
Cd4 T Cells ◽  
E3 Ligase ◽  
Lung Cancer Cells ◽  
Mouse Lung ◽  
Control Group ◽  
Hypoxia Group

Radiofrequency ablation produces a heat-tolerance effect and increases HIF-1αp, and HSP70 expression is distributed in the lesion, but whether HSP70 mediates HIF-1α SUMOylation in lung cancer cells remains unclear. Mouse lung cancer LLC cells were cultured under hypoxia and randomly assigned into control group, heat tolerance group and HSP70 siRNA group followed by analysis of HSP70 and HIF-1α level by real time PCR and Western blot, association of HIF-1α with SUMO-1 and SUMO-2/3 by immunoprecipitation, SENP-1, Ubc9 and E3 ligase expression. CD4 + T cells were isolated and divided into control group, hyperbaric oxygen group, normal temperature hypoxia group, and high temperature hypoxia group followed by measurement of T17 and Treg cell by flow cytometry, and HIF-1α level. HSP70 and HIF-1α level was increased in heat tolerance group and reduced by HSP70 siRNA. Meanwhile, HSP70 siRNA decreased HSP70 binding to SENP-1, Ubc9, and E3 ligase. Heat tolerance group showed decreased SENP-1 expression, increased Ubc9 and E3 ligase expression. HIF-1 bound to SUMO-1, but not SUMO-2/3. HIF-1α expression was increased in CD4+ T cells in treatment group, with significantly increased CD4+ T cells apoptosis and changes of Treg and Th17 compared to control (P < 0 05). HSP70 can promote the heat tolerance effect of lung cancer cells by promoting SUMO-1 expression of HIF-1α; the heat tolerance effect leads to abnormal cellular immune response, which may affect the therapeutic effect.

scholarly journals Targeting focal adhesion kinase in cancer cells and the tumor microenvironment

2020 ◽  
Vol 52 (6) ◽  
pp. 877-886 ◽  
Author(s):  
James M. Murphy ◽  
Yelitza A. R. Rodriguez ◽  
Kyuho Jeong ◽  
Eun-Young Erin Ahn ◽  
Ssang-Taek Steve Lim
Keyword(s):  
Tumor Microenvironment ◽  
Tumor Growth ◽  
Focal Adhesion Kinase ◽  
Cancer Cells ◽  
Focal Adhesion ◽  
Cellular Localization ◽  
Protein Tyrosine Kinase ◽  
Immune Cell ◽  
Preclinical Trials ◽  
Tumor Growth And Metastasis

Abstract Focal adhesion kinase (FAK) is an integrin-associated protein tyrosine kinase that is frequently overexpressed in advanced human cancers. Recent studies have demonstrated that aside from FAK’s catalytic activity in cancer cells, its cellular localization is also critical for regulating the transcription of chemokines that promote a favorable tumor microenvironment (TME) by suppressing destructive host immunity. In addition to the protumor roles of FAK in cancer cells, FAK activity within cells of the TME may also support tumor growth and metastasis through various mechanisms, including increased angiogenesis and vascular permeability and effects related to fibrosis in the stroma. Small molecule FAK inhibitors have demonstrated efficacy in alleviating tumor growth and metastasis, and some are currently in clinical development phases. However, several preclinical trials have shown increased benefits from dual therapies using FAK inhibitors in combination with other chemotherapies or with immune cell activators. This review will discuss the role of nuclear FAK as a driver for tumor cell survival as well as potential therapeutic strategies to target FAK in both tumors and the TME.

scholarly journals Treatment of Lewis lung carcinoma by photodynamic therapy and glucan from barley

Medicina ◽  
2009 ◽  
Vol 45 (6) ◽  
pp. 480 ◽  
Author(s):  
Dalia Akramienė ◽  
Gražina Graželienė ◽  
Janina Didžiapetrienė ◽  
Egidijus Kėvelaitis
Keyword(s):  
Photodynamic Therapy ◽  
Tumor Growth ◽  
Tumor Cells ◽  
Lung Carcinoma ◽  
Lewis Lung Carcinoma ◽  
Specific Interaction ◽  
Control Group ◽  
Complement Receptor ◽  
Lewis Lung ◽  
Complement Receptor 3

Objective. During the photodynamic treatment, complement system is activated and tumor cells are opsonized with iC3b fragment. β-glucans can enhance cytotoxicity of iC3bopsonized cells due to their specific interaction with complement receptor 3 (CR3; CD11b/CD18) on the surface of the effector cells. In contrast to microorganisms, tumor cells lack β-glucan as a surface component and cannot trigger complement receptor 3-dependent cellular cytotoxicity and initiate tumor-killing activity. This mechanism could be induced in the presence of β-glucans. This study aimed at determining the influence of coadministration of β-glucan from barley on the efficacy of photodynamic tumor therapy (PDT). Material and methods. C57 Bl/6 female mice bearing Lewis lung carcinoma were used throughout the study. Mice were randomized into groups (15 in each group) and exposed to the treatment with intravenous Photofrin injection (dose, 10 mg/kg) and after 24 h following laser illumination, or with oral administration of β-glucan from barley at a dose of 400 μg/mouse per day up to 5 days, or with their combination. Tumor growth dynamics and survival of the treated and untreated mice were monitored. Results. Tumor volume in all treated groups was significantly lower (P<0.001) than that in the control group. The most effective tumor growth suppression (P=0.033) was achieved in mice treated with combination of PDT and β-glucan from barley as compared with PDT alone. The best survival was achieved in the same group, but difference was not significant as compared to the control group (P=0.143) and to PDT alone group (P=0.319). Conclusions. The present study demonstrates that coadministration of β-glucan from barley can enhance efficacy of photodynamic therapy.

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