Rapid identification of specific DNA aptamers precisely targeting CD33 positive leukemia cells through a paired cell-based approach

2019 ◽  
Vol 7 (3) ◽  
pp. 938-950 ◽  
Author(s):  
Chang Yang ◽  
Yun Wang ◽  
Ming Hua Ge ◽  
Yu Jie Fu ◽  
Rui Hao ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Anticancer Drugs ◽  
Rapid Identification ◽  
Leukemia Cells ◽  
Dna Aptamers ◽  
Paired Cell

Aptamer S30 selected using modified paired cell-based approach can precisely target CD33-positive cancer cells and deliver anticancer drugs.

scholarly journals Intrinsic growth heterogeneity of mouse leukemia cells underlies differential susceptibility to a growth-inhibiting anticancer drug

2020 ◽  
Author(s):  
Akihisa Seita ◽  
Hidenori Nakaoka ◽  
Reiko Okura ◽  
Yuichi Wakamoto
Keyword(s):  
Cancer Cells ◽  
Anticancer Drugs ◽  
Cancer Cell ◽  
Anticancer Drug ◽  
Differential Susceptibility ◽  
Leukemia Cells ◽  
Continuous Exposure ◽  
Phenotypic Differences ◽  
Cell Lineages ◽  
Slow Cycling

AbstractCancer cell populations consist of phenotypically heterogeneous cells. Growing evidence suggests that pre-existing phenotypic differences among cancer cells correlate with differential susceptibility to anticancer drugs and eventually lead to a relapse. Such phenotypic differences can arise not only externally driven by the environmental heterogeneity around individual cells but also internally by the intrinsic fluctuation of cells. However, the quantitative characteristics of intrinsic phenotypic heterogeneity emerging even under constant environments and their relevance to drug susceptibility remain elusive. Here we employed a microfluidic device, mammalian mother machine, for studying the intrinsic heterogeneity of growth dynamics of mouse lymphocytic leukemia cells (L1210) across tens of generations. The generation time of this cancer cell line had a distribution with a long tail and a heritability across generations. We determined that a minority of cell lineages exist in a slow-cycling state for multiple generations. These slow-cycling cell lineages had a higher chance of survival than the fast-cycling lineages under continuous exposure to the anticancer drug Mitomycin C. This result suggests that heritable heterogeneity in cancer cells’ growth in a population influences their susceptibility to anticancer drugs.

scholarly journals Intrinsic growth heterogeneity of mouse leukemia cells underlies differential susceptibility to a growth-inhibiting anticancer drug

PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0236534
Author(s):  
Akihisa Seita ◽  
Hidenori Nakaoka ◽  
Reiko Okura ◽  
Yuichi Wakamoto
Keyword(s):  
Cancer Cells ◽  
Anticancer Drugs ◽  
Cancer Cell ◽  
Anticancer Drug ◽  
Differential Susceptibility ◽  
Leukemia Cells ◽  
Continuous Exposure ◽  
Phenotypic Differences ◽  
Cell Lineages ◽  
Slow Cycling

Cancer cell populations consist of phenotypically heterogeneous cells. Growing evidence suggests that pre-existing phenotypic differences among cancer cells correlate with differential susceptibility to anticancer drugs and eventually lead to a relapse. Such phenotypic differences can arise not only externally driven by the environmental heterogeneity around individual cells but also internally by the intrinsic fluctuation of cells. However, the quantitative characteristics of intrinsic phenotypic heterogeneity emerging even under constant environments and their relevance to drug susceptibility remain elusive. Here we employed a microfluidic device, mammalian mother machine, for studying the intrinsic heterogeneity of growth dynamics of mouse lymphocytic leukemia cells (L1210) across tens of generations. The generation time of this cancer cell line had a distribution with a long tail and a heritability across generations. We determined that a minority of cell lineages exist in a slow-cycling state for multiple generations. These slow-cycling cell lineages had a higher chance of survival than the fast-cycling lineages under continuous exposure to the anticancer drug Mitomycin C. This result suggests that heritable heterogeneity in cancer cells’ growth in a population influences their susceptibility to anticancer drugs.

Cytotoxic Effect of the Combination of Gemcitabine and Atorvastatin Loaded in Microemulsion on the HCT116 Colon Cancer Cells

2017 ◽  
Vol 9 (2) ◽  
Author(s):  
Mayson H. Alkhatib ◽  
Dalal Al-Saedi ◽  
Wadiah S. Backer
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Anticancer Drugs ◽  
Therapeutic Potential ◽  
Morphological Changes ◽  
In Vitro Study ◽  
Colon Cancer Cells ◽  
Apoptosis Detection ◽  
Hct116 Cells

The combination of anticancer drugs in nanoparticles has great potential as a promising strategy to maximize efficacies by eradicating resistant, reduce the dosage of the drug and minimize toxicities on the normal cells. Gemcitabine (GEM), a nucleoside analogue, and atorvastatin (ATV), a cholesterol lowering agent, have shown anticancer effect with some limitations. The objective of this in vitro study was to evaluate the antitumor activity of the combination therapy of GEM and ATVencapsulated in a microemulsion (ME) formulation in the HCT116 colon cancer cells. The cytotoxicity and efficacy of the formulation were assessed by the 3- (4,5dimethylthiazole-2-yl)-2,5-diphyneltetrazolium bromide (MTT) assay. The mechanism of cell death was examined by observing the morphological changes of treated cells under light microscope, identifying apoptosis by using the ApopNexin apoptosis detection kit, and viewing the morphological changes in the chromatin structure stained with 4′,6-diamidino-2-phenylindole (DAPI) under the inverted fluorescence microscope. It has been found that reducing the concentration of GEM loaded on ME (GEM-ME) from 5μM to 1.67μM by combining it with 3.33μM of ATV in a ME formulation (GEM/2ATV-ME) has preserved the strong cytotoxicity of GEM-ME against HCT116 cells. The current study proved that formulating GEM with ATV in ME has improved the therapeutic potential of GEM and ATV as anticancer drugs.

scholarly journals Bioinformatic Analysis of the Nicotinamide Binding Site in Poly(ADP-Ribose) Polymerase Family Proteins

Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1201
Author(s):  
Garri Manasaryan ◽  
Dmitry Suplatov ◽  
Sergey Pushkarev ◽  
Viktor Drobot ◽  
Alexander Kuimov ◽  
...  
Keyword(s):  
Molecular Modeling ◽  
Cancer Therapy ◽  
Adverse Effects ◽  
Binding Site ◽  
Cancer Cells ◽  
Anticancer Drugs ◽  
Bioinformatic Analysis ◽  
Parp Inhibitors ◽  
Functional Region ◽  
D Loop

The PARP family consists of 17 members with diverse functions, including those related to cancer cells’ viability. Several PARP inhibitors are of great interest as innovative anticancer drugs, but they have low selectivity towards distinct PARP family members and exert serious adverse effects. We describe a family-wide study of the nicotinamide (NA) binding site, an important functional region in the PARP structure, using comparative bioinformatic analysis and molecular modeling. Mutations in the NA site and D-loop mobility around the NA site were identified as factors that can guide the design of selective PARP inhibitors. Our findings are of particular importance for the development of novel tankyrase (PARPs 5a and 5b) inhibitors for cancer therapy.

scholarly journals Surmounting tumor resistance to metallodrugs by co-loading a metal complex and siRNA in nanoparticles

2021 ◽  
Vol 12 (12) ◽  
pp. 4547-4556
Author(s):  
Hongzhi Qiao ◽  
Lei Zhang ◽  
Dong Fang ◽  
Zhenzhu Zhu ◽  
Weijiang He ◽  
...  
Keyword(s):  
Rna Interference ◽  
Metal Complex ◽  
Cancer Cells ◽  
Anticancer Drugs ◽  
Tumor Resistance ◽  
Cu Complex

Bcl-2-related tumor resistance to anticancer drugs can be overcome by silencing the cellular Bcl-2 gene via RNA interference. The realization of the goal is exemplified by delivering Bcl-2 siRNA and a tumor-resistant Cu complex to cancer cells with an ATP-responsive nanocarrier.

Neferine increases sensitivities to multiple anticancer drugs via downregulation of Bcl-2 expression in renal cancer cells

2022 ◽  
Author(s):  
Eun-Ae Kim ◽  
Ji Hoon Jang ◽  
Eon-Gi Sung ◽  
In-Hwan Song ◽  
Joo-Young Kim ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Anticancer Drugs ◽  
Renal Cancer

Circadian Timekeeping in Anticancer Therapeutics: An Emerging Vista of Chronopharmacology Research

2021 ◽  
Vol 22 ◽  
Author(s):  
Alekhya Puppala ◽  
Sourbh Rankawat ◽  
Sandipan Ray
Keyword(s):  
Drug Metabolism ◽  
Circadian Clock ◽  
Cancer Cells ◽  
Anticancer Drugs ◽  
Cancer Biology ◽  
Anticancer Therapy ◽  
Time Of Day ◽  
Circadian Regulation ◽  
Cancer Management ◽  
Anticancer Therapeutics

Background: Intrinsic rhythms in host and cancer cells play an imperative role in tumorigenesis and anticancer therapy. Circadian medicine in cancer is principally reliant on the control of growth and development of cancer cells or tissues by targeting the molecular clock and implementing time-of-day-based anticancer treatments for therapeutic improvements. In recent years, based on extensive high-throughput studies, we witnessed the arrival of several drugs and drug-like compounds that can modulate circadian timekeeping for therapeutic gain in cancer management. Objective: This perspective article intends to illustrate the current trends in circadian medicine in cancer, focusing on clock-modulating pharmacological compounds and circadian regulation of anticancer drug metabolism and efficacy. Scope and Approach: Considering the critical roles of the circadian clock in metabolism, cell signaling, and apoptosis, chronopharmacology research is exceedingly enlightening for understanding cancer biology and improving anticancer therapeutics. In addition to reviewing the relevant literature, we investigated the rhythmic expression of molecular targets for many anticancer drugs frequently used to treat different cancer types. Key Findings and Conclusion: There are adequate empirical pieces of evidence supporting circadian regulation of drug metabolism, transport, and detoxification. Administration of anticancer drugs at specific dosing times can improve their effectiveness and reduce the toxic effects. Moreover, pharmacological modulators of the circadian clock could be used for targeted anticancer therapeutics such as boosting circadian rhythms in the host can markedly reduce the growth and viability of tumors. All in all, precision chronomedicine can offer multiple advantages over conventional anticancer therapy.

scholarly journals Drug-free albumin-triggered sensitization of cancer cells to anticancer drugs

2019 ◽  
Vol 293 ◽  
pp. 84-93 ◽  
Author(s):  
Lian Li ◽  
Jiyuan Yang ◽  
Sirima Soodvilai ◽  
Jiawei Wang ◽  
Praneet Opanasopit ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Anticancer Drugs ◽  
Drug Free

Modulating the cellular uptake of platinum drugs with glycopolymers

2016 ◽  
Vol 7 (5) ◽  
pp. 1031-1036 ◽  
Author(s):  
Aydan Dag ◽  
Manuela Callari ◽  
Hongxu Lu ◽  
Martina H. Stenzel
Keyword(s):  
Cancer Cells ◽  
Anticancer Drugs ◽  
Cellular Uptake ◽  
Platinum Drugs ◽  
Target Cancer

The therapeutic potency of platinum-based anticancer drugs can be substantially improved through the use of fructose-coated nanocarrier systems to target cancer cells efficiently.

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