Millimeter waves non-thermal effect on human lung cancer cells

Therapeutically effective treatments of cancer are limited. To calibrate the efficiency of the novel technique we recently discovered to modulate cancer cell viability using tuned electromagnetic fields; H1299 human lung cancer cells were irradiated in a sweeping regime of W-band (75-105 GHz) millimeter waves (MMW) at 0.2 mW/cm2 (2 W/m2). Effects on cell morphology, cell death and senescence were examined and compared to that of non-tumorigenic MCF-10A human epithelial cells. MMW irradiation led to alterations of cell and nucleus morphology of H1299 cells, significantly increasing mortality and senescence over 14 days of observation. Extended irradiation of 10 minutes duration resulted in complete death of exposed H1299 cell population within two days, while healthy MCF-10A cells remained unaffected even after 16 minutes of irradiation under the same conditions. Irradiation effects were observed to be specific to MMW treated H1299 cells and absent in the control group of non-irradiated cells. MMW irradiation affected nuclear morphology of H1299 cells only and not of the immortalized MCF-10A cells. Irradiation with low intensity MMW shows an antitumor effect on H1299 lung cancer cells. This method provides a novel treatment modality enabling targeted specificity for various types of cancers.

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W-Band Millimeter Waves Targeted Mortality of H1299 Human Lung Cancer Cells without Affecting Non-tumorigenic MCF-10A Human Epithelial Cells In Vitro

10.20944/preprints202005.0296.v1 ◽

2020 ◽

Author(s):

Konstantin Komoshvili ◽

Katya Israel ◽

Jacob Levitan ◽

Asher Yahalom ◽

Ayan Barbora ◽

...

Keyword(s):

Lung Cancer ◽

Epithelial Cells ◽

Cancer Cells ◽

Cell Morphology ◽

Millimeter Waves ◽

Human Lung ◽

Lung Cancer Cells ◽

Human Lung Cancer ◽

W Band ◽

Human Lung Cancer Cells

Therapeutically effective treatments of cancer are limited. To calibrate the efficiency of the novel technique we recently discovered to modulate cancer cell viability using tuned electromagnetic fields; H1299 human lung cancer cells were irradiated in a sweeping regime of W-band (75-105 GHz) millimeter waves (MMW) at 0.2 mW/cm2 (2 W/m2). Effects on cell morphology, cell death and senescence were examined and compared to that of non-tumorigenic MCF-10A human epithelial cells. MMW irradiation led to alterations of cell and nucleus morphology of H1299 cells, significantly increasing mortality and senescence over 14 days of observation. Extended irradiation of 10 minutes duration resulted in complete death of exposed H1299 cell population within two days, while healthy MCF-10A cells remained unaffected even after 16 minutes of irradiation under the same conditions. Irradiation effects were observed to be specific to MMW treated H1299 cells and absent in the control group of non-irradiated cells. MMW irradiation did not affect cell morphology of immortalized MCF-10A cells. Irradiation with low intensity MMW shows an antitumor effect on H1299 lung cancer cells. This method provides a novel treatment modality enabling targeted specificity for various types of cancers.

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W-Band Millimeter Waves Targeted Mortality of H1299 Human Lung Cancer Cells without Affecting Non-Tumorigenic MCF-10A Human Epithelial Cells In Vitro

Applied Sciences ◽

10.3390/app10144813 ◽

2020 ◽

Vol 10 (14) ◽

pp. 4813

Author(s):

Konstantin Komoshvili ◽

Katya Israel ◽

Jacob Levitan ◽

Asher Yahalom ◽

Ayan Barbora ◽

...

Keyword(s):

Lung Cancer ◽

Epithelial Cells ◽

Cancer Cells ◽

Millimeter Waves ◽

Human Lung ◽

Lung Cancer Cells ◽

Human Lung Cancer ◽

Human Epithelial Cells ◽

W Band ◽

Human Lung Cancer Cells

Therapeutically effective treatments of cancer are limited. To calibrate the efficiency of the novel technique we recently discovered to modulate cancer cell viability using tuned electromagnetic fields; H1299 human lung cancer cells were irradiated in a sweeping regime of W-band (75–105 GHz) millimeter waves (MMW) at 0.2 mW/cm2 (2 W/m2). Effects on cell morphology, cell death and senescence were examined and compared to that of non-tumorigenic MCF-10A human epithelial cells. MMW irradiation led to alterations of cell and nucleus morphology of H1299 cells, significantly increasing mortality and senescence over 14 days of observation. Extended irradiation of 10 min duration resulted in complete death of exposed H1299 cell population within two days, while healthy MCF-10A cells remained unaffected even after 16 min of irradiation under the same conditions. Irradiation effects were observed to be specific to MMW treated H1299 cells and absent in the control group of non-irradiated cells. MMW irradiation affected nuclear morphology of H1299 cells only and not of the immortalized MCF-10A cells. Irradiation with low intensity MMW shows an antitumor effect on H1299 lung cancer cells. This method provides a novel treatment modality enabling targeted specificity for various types of cancers.

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Anticancer activity of peptide extracted from edible mushroom; Lentinus squarrosulus in human lung cancer cells

Planta Medica ◽

10.1055/s-0036-1596829 ◽

2016 ◽

Vol 81 (S 01) ◽

pp. S1-S381

Author(s):

S Sumkhemthong ◽

M Suksomtip ◽

P Chanvorachote ◽

C Chaotham

Keyword(s):

Lung Cancer ◽

Anticancer Activity ◽

Cancer Cells ◽

Human Lung ◽

Edible Mushroom ◽

Lung Cancer Cells ◽

Human Lung Cancer ◽

Human Lung Cancer Cells

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Inhibitory effects of Actinidia Chinensis planch root extracts (acRoots) on human lung cancer cells through retinoic acid receptor beta

Molecular and Cellular Therapies ◽

10.26781/2052-8426-2017-02 ◽

2017 ◽

Vol 5 (1) ◽

Cited By ~ 1

Author(s):

Lingyan Wang ◽

Jiayun Hou ◽

Minghuan Zheng ◽

Lin Shi

Keyword(s):

Lung Cancer ◽

Cancer Cells ◽

Human Lung ◽

Retinoic Acid Receptor ◽

Lung Cancer Cells ◽

Human Lung Cancer ◽

Inhibitory Effects ◽

The Core ◽

Human Lung Cancer Cells ◽

Receptor Beta

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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EFFECTS OF OPIOIDS AND NICOTINE ON APOPTOSIS IN HUMAN LUNG CANCER CELLS

Analgesia ◽

10.3727/107156995819564068 ◽

1995 ◽

Vol 1 (4) ◽

pp. 548-552

Author(s):

Rhoda Maneckjee ◽

Kathleen Dehen ◽

John D. Minna

Keyword(s):

Lung Cancer ◽

Cancer Cells ◽

Human Lung ◽

Lung Cancer Cells ◽

Human Lung Cancer ◽

Human Lung Cancer Cells

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SP1 Mediates MRP1 Upregulation and Multi-Drug Resistance in Human Lung Cancer Cells

SSRN Electronic Journal ◽

10.2139/ssrn.3427292 ◽

2019 ◽

Author(s):

Shuli Shao ◽

Yunjianan Feng ◽

Yue Xiao ◽

Yan Li ◽

Weiwei Zhang ◽

...

Keyword(s):

Lung Cancer ◽

Drug Resistance ◽

Cancer Cells ◽

Human Lung ◽

Lung Cancer Cells ◽

Human Lung Cancer ◽

Multi Drug Resistance ◽

Human Lung Cancer Cells

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Fas Ligand Enhances Apoptosis of Human Lung Cancer Cells Cotreated with RIG-I-like Receptor Agonist and Radiation

Current Cancer Drug Targets ◽

10.2174/1568009620666200115161717 ◽

2020 ◽

Vol 20 (5) ◽

pp. 372-381

Author(s):

Yoshiaki Sato ◽

Hironori Yoshino ◽

Eichi Tsuruga ◽

Ikuo Kashiwakura

Keyword(s):

Lung Cancer ◽

Cell Surface ◽

Cancer Cells ◽

Fas Ligand ◽

Human Lung ◽

Lung Cancer Cells ◽

Poly I:C ◽

Human Lung Cancer ◽

Human Lung Cancer Cells ◽

Induced Apoptosis

Background: Retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) play key roles in the antiviral response, but recent works show that RLR activation elicits anticancer activity as well, including apoptosis. Previously, we demonstrated that the anticancer activity of the RLR agonist Poly(I:C)-HMW/LyoVec™ [Poly(I:C)-HMW] against human lung cancer cells was enhanced by cotreatment with ionizing radiation (IR). In addition, cotreatment with Poly(I:C)-HMW and IR induced apoptosis in a Fas-independent manner, and increased Fas expression on the cell surface. Objective: The current study investigated the resultant hypothesis that Fas ligand (FasL) may enhance apoptosis in lung cancer cells cotreated with Poly(I:C)-HMW+IR. Methods: FasL was added into culture medium at 24 h following cotreatment with Poly(I:C)- HMW+IR, after upregulation of cell surface Fas expression on human lung cancer cells A549 and H1299 have already been discussed. Results: FasL enhanced the apoptosis of A549 and H1299 cells treated with Poly(I:C)-HMW+IR. Similarly, IR alone - and not Poly(I:C)-HMW - resulted in the upregulation of cell surface Fas expression followed by a high response to FasL-induced apoptosis, thus suggesting that the high sensitivity of cells treated with Poly(I:C)-HMW+IR to FasL-induced apoptosis resulted from the cellular response to IR. Finally, knockdown of Fas by siRNA confirmed that the high response of treated cells to FasL-induced apoptosis is dependent on Fas expression. Conclusion: In summary, the present study indicates that upregulated Fas expression following cotreatment with Poly(I:C)-HMW and IR is responsive to FasL-induced apoptosis, and a combination of RLR agonist, IR, and FasL could be a potential promising cancer therapy.

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Isoorientin Decreases Cell Migration via Decreasing Functional Activity and Molecular Expression of Proton-Linked Monocarboxylate Transporters in Human Lung Cancer Cells

The American Journal of Chinese Medicine ◽

10.1142/s0192415x20500111 ◽

2020 ◽

Vol 48 (01) ◽

pp. 201-222

Author(s):

Hsu-Kai Huang ◽

Shin-Yi Lee ◽

Shu-Fen Huang ◽

Yu-San Lin ◽

Shih-Chi Chao ◽

...

Keyword(s):

Lung Cancer ◽

Cell Migration ◽

Lung Adenocarcinoma ◽

Cell Viability ◽

Cancer Cells ◽

Functional Activity ◽

Human Lung ◽

Lung Cancer Cells ◽

Human Lung Cancer ◽

Human Lung Cancer Cells

Aggressive tumor cells mainly rely on glycolysis, and further release vast amounts of lactate and protons by monocarboxylate transporter (MCT), which causes a higher intracellular pH (pHi) and acidic extracellular pH. Isoorientin, a principle flavonoid compound extracted from several plant species, shows various pharmacological activities. However, effects of isoorientin on anticancer and MCT await to explore in human lung cancer cells. Human lung cancer tissues were obtained from cancer patients undergoing surgery, while the human lung adenocarcinoma cells (A549) were bought commercially. Change of pHi was detected by microspectrofluorometry method with a pH-sensitive fluorescent dye, BCECF. MTT and wound-healing assay were used to detect the cell viability and migration, respectively. Western blot techniques and immunocytochemistry staining were used to detect the protein expression. Our results indicated that the expression of MCTs1/4 and CD147 were upregulated significantly in human lung tissues. In experiments of A549 cells, under HEPES-buffer, the resting pHi was 7.47, and isoorientin (1–300[Formula: see text][Formula: see text]M) inhibited functional activity of MCT concentration-dependently (up to [Formula: see text]%). Pretreatment with isoorientin (3–100[Formula: see text][Formula: see text]M) for 24[Formula: see text]h, MCT activity and cell migration were significantly inhibited ([Formula: see text]% and [Formula: see text]%, respectively), while the cell viability was not affected. Moreover, the expression of MCTs1/4, CD147, and matrix metalloproteinase (MMP) 2/9 were significantly down regulated. In summary, MCTs1/4 and CD147 are significantly upregulated in human lung adenocarcinoma tissues, and isoorientin inhibits cells-migration by inhibiting activity/expression of MCTs1/4 and MMPs2/9 in human lung cancer cells. These novel findings suggest that isoorientin could be a promising pharmacological agent for lung cancer.

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