Showing 161 - 180 results of 1,456 for search '"cancer cells"', query time: 0.13s Refine Results
  1. 161

    Sigma1 inhibitor suppression of adaptive immune resistance mechanisms mediated by cancer cell derived extracellular vesicles by Paola A. Castagnino, Derick A. Haas, Luca Musante, Nathalia A. Tancler, Bach V. Tran, Rhonda Kean, Alexandra R. Steck, Luis A. Martinez, Elahe A. Mostaghel, D. Craig Hooper, Felix J. Kim

    Published 2025-12-01
    “…PD-L1 can also be incorporated into cancer cell-derived extracellular vesicles (EVs), and EV-associated PD-L1 can inactivate T-cells within the tumor microenvironment. …”
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  2. 162
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    Exploring the interactions of rapamycin with target receptors in A549 cancer cells: insights from molecular docking analysis by Sanjeev K. Ganesh, C. Subathra Devi

    Published 2025-01-01
    “…Also reports on the binding of rapamycin to cancer cell receptors are limited to the serine/threonine protein kinase mTORC1. …”
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  5. 165

    Sesquiterpenes α-humulene and β-caryophyllene oxide enhance the efficacy of 5-fluorouracil and oxaliplatin in colon cancer cells by Ambrož Martin, Šmatová Markéta, Šadibolová Michaela, Pospíšilová Eva, Hadravská Pavlína, Kašparová Michaela, Skarková Veronika Hanušová, Králová Věra, Skálová Lenka

    Published 2019-03-01
    “…The results show significant ability of HUM and especially of CAO to enhance the anti-proliferative effects of FU and OxPt in cancer cell lines Caco-2 and SW-620. On the other hand, VAL and NER are ineffective. …”
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  6. 166
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    Nano–bio surface interactions, cellular internalisation in cancer cells and e‐data portals of nanomaterials: A review by Ram Dhan Yadav, Abha Chaudhary

    Published 2021-08-01
    “…Thus, the present review emphasises the impact of coated, uncoated NMs, size and charge, nature of proteins on nano–bio surface interactions and on internalisation with specific focus on cancer cells. The increased activity of NPs may also result in toxicity on health and environment, thus emphasis should be given to assess the toxicity of NMs in the medical field. …”
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  8. 168

    Assessment of Morphological Changes in Breast Cancer Cells Following X-Ray Radiation Utilizing Digital Holographic Microscopy by Zeinab Hormozi-Moghaddam, Seyedeh Mona Taheri, Reza Paydar, Ali Neshasteh-Riz, Vahideh Farzam Rad, Mohadeseh Shaghaghi

    Published 2025-01-01
    “…The primary objective of this investigation is to scrutinize the capability of a digital holographic microscope in assessing the morphological transformations of cancer cells exposed to X-ray radiation. Materials and Methods: The Michigan Cancer Foundation-7 (MCF7) cell line underwent exposure to X-ray radiation, administered in a singular fraction at a dose of 2 Gy. …”
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  11. 171

    Effects of Pleurotus Eryngii (DC.) Quél. Mushroom Extracts on Cell Proliferation in Breast and Colon Cancer Cell Lines by Mehmet Ay, Hakan Allı, Alper Önder, Gülce Davutlar, Ferah Cömert Önder

    Published 2024-09-01
    “…Then, breast (MDA-MB-231, BT-549, BT-20, MCF-7) and colon (HT-29) cancer cell lines were treated with the extracts in increasing concentrations (0.05-0.5 mg/mL) for 48 h. …”
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  12. 172

    GTSE1 Facilitates the Malignant Phenotype of Lung Cancer Cells via Activating AKT/mTOR Signaling by Fan Zhang, Jingfei Meng, Hong Jiang, Xing Feng, Dongshan Wei, Wen Meng

    Published 2021-01-01
    “…Ectopic expression of GTSE1 in lung cancer cells significantly increased while knockdown of GTSE1 decreased cell proliferation, cell migration, and cell invasion in H460 and A549 cells. …”
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  13. 173

    miR-149 Inhibits Non-Small-Cell Lung Cancer Cells EMT by Targeting FOXM1 by Yang Ke, Weiyong Zhao, Jie Xiong, Rubo Cao

    Published 2013-01-01
    “…MicroRNAs (miRNAs) have been implied to play crucial roles for epithelial-to-mesenchymal transition (EMT) of non-small-cell lung cancer cells (NSCLC cells). Here we found that the expression of miR-149, downregulated in lung cancer, was inversely correlated with invasive capability and the EMT phenotype of NSCLC cells. miR-149 inhibited EMT in NSCLC cells. …”
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  14. 174

    Investigating the Expression of c-Myc and BIRC5 in TRAIL and PBOX-15 treated Metastatic Prostate Cancer Cells by Corinne Kai Leng Chew, Hannah O'Toole, Daniela M Zisterer, Seema M. Nathwani, Jade K. Pollock

    Published 2024-12-01
    “…Overexpression of c-Myc and BIRC5 has been reported in prostate cancer cells which contribute to the development of the tumour environment. …”
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  15. 175

    High Expression of UPK3A Promotes the Progression of Gastric Cancer Cells by Inactivating p53 Pathway by Deliang Xu, Jing Guo, Hongwei Xu

    Published 2022-01-01
    “…UPK3A was highly expressed in human gastric cancer cell lines compared to that in a normal human gastric epithelial cell line. …”
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  16. 176

    Autophagic flux-lipid droplet biogenesis cascade sustains mitochondrial fitness in colorectal cancer cells adapted to acidosis by Xiaojie Liu, Xue Sun, Wenqing Mu, Yanan Li, Wenqing Bu, Tingting Yang, Jia Zhang, Rui Liu, Jiayu Ren, Jin Zhou, Peishan Li, Yufang Shi, Changshun Shao

    Published 2025-01-01
    “…Thus, our results demonstrate that the cascade of autophagic flux and LD formation plays an essential role in sustaining mitochondrial fitness to promote cancer cell survival under chronic acidosis. Our findings provide insight into the pro-survival metabolic plasticity in cancer cells under microenvironmental or therapeutic stress and imply that this pro-survival cascade may potentially be targeted in cancer therapy.…”
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  17. 177

    Dataset of transcriptomic changes induced by naringenin treatment in MCF-7 breast cancer cellsGene Expression Omnibus by Van T. Hoang, Mackenzie L. Hawes, Jack R. Elliott, Steven Elliott, Binghao Zou, Stephen M. Boué, Brian G. Rowan, Bridgette M. Collins-Burow, Jorge A. Belgodere, Muralidharan Anbalagan, Elizabeth C. Martin, Matthew E. Burow

    Published 2025-04-01
    “…Pathway analysis included in our dataset shows upregulation of genes associated with estrogen signaling and epithelial-to-mesenchymal transition in breast cancer cells treated with naringenin.…”
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    CPSF1 inhibition promotes widespread use of intergenic polyadenylation sites and impairs glycolysis in prostate cancer cells by Kiel T. Tietz, Braedan M. McCluskey, Conor R. Miller, Yingming Li, Sarah A. Munro, Scott M. Dehm

    Published 2025-01-01
    “…Knockdown of CPSF1 selectively inhibited the growth of prostate cancer cells and reduced glycolytic output. Evaluating the changes in global poly(A) site usage in prostate cancer cells following CPSF1 knockdown revealed widespread usage of intergenic poly(A) sites distal to annotated 3′ UTRs, which lengthened 3′ UTRs and decreased levels of thousands of mRNAs, including key glycolysis genes. …”
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