scholarly journals Probing biotin receptors in cancer cells with rationally designed fluorogenic squaraine dimers

2020 ◽  
Vol 11 (31) ◽  
pp. 8240-8248 ◽  
Author(s):  
Kyong T. Fam ◽  
Mayeul Collot ◽  
Andrey S. Klymchenko
Keyword(s):  
Cancer Cells ◽  
Rational Design ◽  
Fluorogenic Probe ◽  
Cancerous Cells

Rational design of self-quenched squaraine dimers bearing biotin yielded a bright fluorogenic probe that can distinguish cancerous from non-cancerous cells.

Tubulin Proteins in Cancer Resistance: A Review

2020 ◽  
Vol 21 (3) ◽  
pp. 178-185 ◽  
Author(s):  
Mohammad Amjad Kamal ◽  
Maryam Hassan Al-Zahrani ◽  
Salman Hasan Khan ◽  
Mateen Hasan Khan ◽  
Hani Awad Al-Subhi ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cancer Cells ◽  
High Rate ◽  
Vinca Alkaloids ◽  
Cancer Resistance ◽  
New Approach ◽  
Natural Sources ◽  
Cell Cycle Genes ◽  
Cancerous Cells ◽  
Β Tubulin

Cancer cells are altered with cell cycle genes or they are mutated, leading to a high rate of proliferation compared to normal cells. Alteration in these genes leads to mitosis dysregulation and becomes the basis of tumor progression and resistance to many drugs. The drugs which act on the cell cycle fail to arrest the process, making cancer cell non-responsive to apoptosis or cell death. Vinca alkaloids and taxanes fall in this category and are referred to as antimitotic agents. Microtubule proteins play an important role in mitosis during cell division as a target site for vinca alkaloids and taxanes. These proteins are dynamic in nature and are composed of α-β-tubulin heterodimers. β-tubulin specially βΙΙΙ isotype is generally altered in expression within cancerous cells. Initially, these drugs were very effective in the treatment of cancer but failed to show their desired action after initial chemotherapy. The present review highlights some of the important targets and their mechanism of resistance offered by cancer cells with new promising drugs from natural sources that can lead to the development of a new approach to chemotherapy.

scholarly journals Landscape of Chimeric RNAs in Non-Cancerous Cells

Genes ◽  
2021 ◽  
Vol 12 (4) ◽  
pp. 466
Author(s):  
Chen Chen ◽  
Samuel Haddox ◽  
Yue Tang ◽  
Fujun Qin ◽  
Hui Li
Keyword(s):  
Cancer Cells ◽  
Cell Lines ◽  
Drug Targets ◽  
Neoplastic Cell ◽  
Multiple Cancer ◽  
Chimeric Rnas ◽  
Healthy Donors ◽  
Cancer Types ◽  
Chimeric Rna ◽  
Cancerous Cells

Gene fusions and their products (RNA and protein) have been traditionally recognized as unique features of cancer cells and are used as ideal biomarkers and drug targets for multiple cancer types. However, recent studies have demonstrated that chimeric RNAs generated by intergenic alternative splicing can also be found in normal cells and tissues. In this study, we aim to identify chimeric RNAs in different non-neoplastic cell lines and investigate the landscape and expression of these novel candidate chimeric RNAs. To do so, we used HEK-293T, HUVEC, and LO2 cell lines as models, performed paired-end RNA sequencing, and conducted analyses for chimeric RNA profiles. Several filtering criteria were applied, and the landscape of chimeric RNAs was characterized at multiple levels and from various angles. Further, we experimentally validated 17 chimeric RNAs from different classifications. Finally, we examined a number of validated chimeric RNAs in different cancer and non-cancer cells, including blood from healthy donors, and demonstrated their ubiquitous expression pattern.

An integrin-targeting nanosystem as a carrier of the selenadiazole derivative to induce ROS-mediated apoptosis in bladder cancer cells, from rational design to action mechanisms

2015 ◽  
Vol 3 (48) ◽  
pp. 9374-9382 ◽  
Author(s):  
Yifan Wang ◽  
Wenying Li ◽  
Yahui Yang ◽  
Qinsong Zeng ◽  
Ka-Hing Wong ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Rational Design ◽  
Action Mechanisms ◽  
Bladder Cancer Cells

Herein an integrin-targeting nanosystem is rationally designed and used as a carrier of a selenadiazole derivative to induce ROS-mediated apoptosis in bladder cancer cells.

scholarly journals The “ARTS” of Cell Death in Service of Life: How Do We Force Cancer Cells to Commit Suicide?

2021 ◽  
Vol 9 ◽  
Author(s):  
Sarit Larisch
Keyword(s):  
Cell Death ◽  
Cancer Cells ◽  
Novel Therapy ◽  
The Arts ◽  
Wide Range ◽  
Cell Death Program ◽  
Cancerous Cells ◽  
Critical Process ◽  
Cells Death ◽  
Commit Suicide

Every cell in our body contains a “self-destruction” program. This cell death is a critical process allowing replacement of damaged cells with healthy ones to prevent wide range of diseases. When the cell’s death mechanism gets “stuck” and is not activated, cancer can result. In healthy cells there is a balanced system of proteins, some of which activate the normal death mechanism, and some of which inhibit this process. This is like the system of gas and brakes in a car. Researchers have found that cancer cells lack a protein, called ARTS, which is crucial for activating the cells’ death mechanism. The lack of ARTS causes cancer cells to escape death and become “immortal.” Small ARTS-like molecules have been discovered that can penetrate cancerous cells and reactivate the cell death program, effectively making the cancer cells “commit suicide.” We envision that these ARTS-like molecules will provide novel therapy for cancer.

scholarly journals Targeting cancer cell metabolism with mitochondria-immobilized phosphorescent cyclometalated iridium(iii) complexes

2017 ◽  
Vol 8 (1) ◽  
pp. 631-640 ◽  
Author(s):  
Jian-Jun Cao ◽  
Cai-Ping Tan ◽  
Mu-He Chen ◽  
Na Wu ◽  
De-Yang Yao ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Cancer Cell ◽  
Rational Design ◽  
Cell Metabolism ◽  
Mitochondrial Metabolism ◽  
Cancer Cell Metabolism

We report a rational design and mechanism studies of mitochondria-immobilized iridium(iii) complexes that can kill cancer cells by targeting mitochondrial metabolism.

scholarly journals Electrical Impedance Spectroscopy for Monitoring Chemoresistance of Cancer Cells

Micromachines ◽  
2020 ◽  
Vol 11 (9) ◽  
pp. 832
Author(s):  
Lexi Crowell ◽  
Juan Yakisich ◽  
Brian Aufderheide ◽  
Tayloria Adams
Keyword(s):  
Impedance Spectroscopy ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cellular Response ◽  
Electrical Impedance ◽  
Electrical Impedance Spectroscopy ◽  
Cell Behavior ◽  
Drug Resistant ◽  
Cancerous Cells

Electrical impedance spectroscopy (EIS) is an electrokinetic method that allows for the characterization of intrinsic dielectric properties of cells. EIS has emerged in the last decade as a promising method for the characterization of cancerous cells, providing information on inductance, capacitance, and impedance of cells. The individual cell behavior can be quantified using its characteristic phase angle, amplitude, and frequency measurements obtained by fitting the input frequency-dependent cellular response to a resistor–capacitor circuit model. These electrical properties will provide important information about unique biomarkers related to the behavior of these cancerous cells, especially monitoring their chemoresistivity and sensitivity to chemotherapeutics. There are currently few methods to assess drug resistant cancer cells, and therefore it is difficult to identify and eliminate drug-resistant cancer cells found in static and metastatic tumors. Establishing techniques for the real-time monitoring of changes in cancer cell phenotypes is, therefore, important for understanding cancer cell dynamics and their plastic properties. EIS can be used to monitor these changes. In this review, we will cover the theory behind EIS, other impedance techniques, and how EIS can be used to monitor cell behavior and phenotype changes within cancerous cells.

Rational design of water-dispersible and biocompatible nanoprobes with H2S-triggered NIR emission for cancer cell imaging

2020 ◽  
Vol 8 (28) ◽  
pp. 6013-6016
Author(s):  
Hengyan Liu ◽  
Ge Xu ◽  
Tianli Zhu ◽  
Rongchen Wang ◽  
Jiahui Tan ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Cancer Cell ◽  
Small Molecule ◽  
Rational Design ◽  
Cell Imaging ◽  
Imaging Modality ◽  
Aqueous Solubility ◽  
Water Dispersible ◽  
Nir Emission ◽  
Small Molecule Probe

A nanoprobe with good aqueous solubility and biocompatibility by trapping an H2S-activatable small molecule probe in the interior of surface cross-linked micelles was fabricated for imaging of H2S-rich cancer cells in a dual-color imaging modality.

scholarly journals CCL18 in the Progression of Cancer

2020 ◽  
Vol 21 (21) ◽  
pp. 7955 ◽  
Author(s):  
Jan Korbecki ◽  
Mateusz Olbromski ◽  
Piotr Dzięgiel
Keyword(s):  
Tumor Microenvironment ◽  
Cancer Cells ◽  
Epithelial To Mesenchymal Transition ◽  
M2 Macrophage ◽  
Mesenchymal Transition ◽  
Neoplastic Processes ◽  
Anti Cancer ◽  
Macrophage Subset ◽  
Cancerous Cells ◽  
Worse Prognosis

A neoplastic tumor consists of cancer cells that interact with each other and non-cancerous cells that support the development of the cancer. One such cell are tumor-associated macrophages (TAMs). These cells secrete many chemokines into the tumor microenvironment, including especially a large amount of CCL18. This chemokine is a marker of the M2 macrophage subset; this is the reason why an increase in the production of CCL18 is associated with the immunosuppressive nature of the tumor microenvironment and an important element of cancer immune evasion. Consequently, elevated levels of CCL18 in the serum and the tumor are connected with a worse prognosis for the patient. This paper shows the importance of CCL18 in neoplastic processes. It includes a description of the signal transduction from PITPNM3 in CCL18-dependent migration, invasion, and epithelial-to-mesenchymal transition (EMT) cancer cells. The importance of CCL18 in angiogenesis has also been described. The paper also describes the effect of CCL18 on the recruitment to the cancer niche and the functioning of cells such as TAMs, regulatory T cells (Treg), cancer-associated fibroblasts (CAFs) and tumor-associated dendritic cells (TADCs). The last part of the paper describes the possibility of using CCL18 as a therapeutic target during anti-cancer therapy.

scholarly journals Metabolic cooperation between cancer and non-cancerous stromal cells is pivotal in cancer progression

Tumor Biology ◽  
2018 ◽  
Vol 40 (2) ◽  
pp. 101042831875620 ◽  
Author(s):  
Filipa Lopes-Coelho ◽  
Sofia Gouveia-Fernandes ◽  
Jacinta Serpa
Keyword(s):  
Cancer Cells ◽  
Cancer Progression ◽  
Stromal Cells ◽  
Inflammatory Cells ◽  
Metabolic Adaptation ◽  
Metabolic Cooperation ◽  
Metabolic Remodeling ◽  
Organ Tissue ◽  
Cancerous Cells

The way cancer cells adapt to microenvironment is crucial for the success of carcinogenesis, and metabolic fitness is essential for a cancer cell to survive and proliferate in a certain organ/tissue. The metabolic remodeling in a tumor niche is endured not only by cancer cells but also by non-cancerous cells that share the same microenvironment. For this reason, tumor cells and stromal cells constitute a complex network of signal and organic compound transfer that supports cellular viability and proliferation. The intensive dual-address cooperation of all components of a tumor sustains disease progression and metastasis. Herein, we will detail the role of cancer-associated fibroblasts, cancer-associated adipocytes, and inflammatory cells, mainly monocytes/macrophages (tumor-associated macrophages), in the remodeling and metabolic adaptation of tumors.

scholarly journals Mitochondria-driven elimination of cancer and senescent cells

2019 ◽  
Vol 400 (2) ◽  
pp. 141-148 ◽  
Author(s):  
Sona Hubackova ◽  
Silvia Magalhaes Novais ◽  
Eliska Davidova ◽  
Jiri Neuzil ◽  
Jakub Rohlena
Keyword(s):  
Oxidative Phosphorylation ◽  
Cancer Cells ◽  
Selective Removal ◽  
Mitochondrial Morphology ◽  
Mitochondrial Targeting ◽  
Pharmacological Interventions ◽  
Cancerous Cells ◽  
Efficient Elimination ◽  
Oxidative Insult

AbstractMitochondria and oxidative phosphorylation (OXPHOS) are emerging as intriguing targets for the efficient elimination of cancer cells. The specificity of this approach is aided by the capacity of non-proliferating non-cancerous cells to withstand oxidative insult induced by OXPHOS inhibition. Recently we discovered that mitochondrial targeting can also be employed to eliminate senescent cells, where it breaks the interplay between OXPHOS and ATP transporters that appear important for the maintenance of mitochondrial morphology and viability in the senescent setting. Hence, mitochondria/OXPHOS directed pharmacological interventions show promise in several clinically-relevant scenarios that call for selective removal of cancer and senescent cells.

Sign in / Sign up

Export Citation Format

Share Document