Amphiphilic fluorescent probe self-encored in plasma to detect pH fluctuations in cancer cell membranes

2021 ◽  
Author(s):  
Arup Podder ◽  
Manu M. Joseph ◽  
Shayeri Biswas ◽  
Sanjib Samanta ◽  
Kaustabh K. Maiti ◽  
...  

Newly developed an amphiphilic “turn-on” fluorescent probe (P1CS) enables to distinguish of cancer cells from normal cells through mapping of pH fluctuations in cell-surface.

2018 ◽  
Vol 6 (27) ◽  
pp. 4514-4521 ◽  
Author(s):  
Arup Podder ◽  
Sudipta Senapati ◽  
Pralay Maiti ◽  
Devaraj Kamalraj ◽  
Syed S Jaffer ◽  
...  

A turn-on fluorescent probe (LP1) discriminates cancer cells from normal cells based on expression of phosphatase in lysosomes.


The Analyst ◽  
2019 ◽  
Vol 144 (16) ◽  
pp. 4750-4756 ◽  
Author(s):  
Li Liu ◽  
Rui-Jie Lv ◽  
Jong-Kai Leung ◽  
Qian Zou ◽  
Yue Wang ◽  
...  

A novel near-infrared biothiol-specific fluorescent probe can discriminate cancer cells from normal cells showing great promise for cancer diagnosis.


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Yu-An Chen ◽  
Yong-Da Sie ◽  
Tsung-Yun Liu ◽  
Hsiang-Ling Kuo ◽  
Pei-Yi Chou ◽  
...  

AbstractMetastatic cancer cells are frequently deficient in WWOX protein or express dysfunctional WWOX (designated WWOXd). Here, we determined that functional WWOX-expressing (WWOXf) cells migrate collectively and expel the individually migrating WWOXd cells. For return, WWOXd cells induces apoptosis of WWOXf cells from a remote distance. Survival of WWOXd from the cell-to-cell encounter is due to activation of the survival IκBα/ERK/WWOX signaling. Mechanistically, cell surface epitope WWOX286-299 (repl) in WWOXf repels the invading WWOXd to undergo retrograde migration. However, when epitope WWOX7-21 (gre) is exposed, WWOXf greets WWOXd to migrate forward for merge. WWOX binds membrane type II TGFβ receptor (TβRII), and TβRII IgG-pretreated WWOXf greet WWOXd to migrate forward and merge with each other. In contrast, TβRII IgG-pretreated WWOXd loses recognition by WWOXf, and WWOXf mediates apoptosis of WWOXd. The observatons suggest that normal cells can be activated to attack metastatic cancer cells. WWOXd cells are less efficient in generating Ca2+ influx and undergo non-apoptotic explosion in response to UV irradiation in room temperature. WWOXf cells exhibit bubbling cell death and Ca2+ influx effectively caused by UV or apoptotic stress. Together, membrane WWOX/TβRII complex is needed for cell-to-cell recognition, maintaining the efficacy of Ca2+ influx, and control of cell invasiveness.


Author(s):  
Madheswaran Suresh ◽  
Malarvizhi Gurusamy ◽  
Natarajan Sudhakar

<p>Immune surveillance is a mechanism where cells and tissues are watched constantly by ever alerted immune system. Most incipient cancer cells are recognized and eliminated by the immune surveillance mechanism, but still tumors have the ability to evade immune surveillance and immunological killing. One greater arm that tumor use to evade immune surveillance, is by expressing anti-phagocytic signal (CD47). Here we present a provocative hypothesis where cancer cells are removed alive by phagocytic cell (DC). That in turn will elicit effective and higher immunogenic condition. All this could be possible by addition pro-phagocytic signal (PtdSer) over cancer cell surface (Breast Cancer), that mask the presence of anti-phagocytic signal (CD47). In other words, adding eat me signal (PtdSer) over the breast cancer cell surface that mask the presence of don’t eat me signal or anti-phagocytic signal present in breast cancer cell surface. This could be possible by using bi-specific antibody, conjugated to PEG-modified liposomes, which carry (PtdSer) pro-phagocytic signal (or) eat me signal, which target both CD47 and EGFRVIII on breast carcinoma. The simultaneous masking of anti-phagocytic signal, and adding of pro–phagocytic signal over cancer cell, will enhance the phagocytic clearance of live tumor cell and elicit immunological killing.</p>


2020 ◽  
Vol 11 (36) ◽  
pp. 9875-9883 ◽  
Author(s):  
Soo Yeon Kim ◽  
Arup Podder ◽  
Hyunseung Lee ◽  
Youn-Joo Cho ◽  
Eun Hee Han ◽  
...  

A self-assembled amphiphilic fluorescent probe allows pH-fluctuations within cancer cells and tumour tissues to be readily detected.


2019 ◽  
Vol 7 (43) ◽  
pp. 6822-6827 ◽  
Author(s):  
Fanpeng Kong ◽  
Ying Li ◽  
Chao Yang ◽  
Xiao Li ◽  
Junlin Wu ◽  
...  

A dual-enzyme-responsive probe, CNN, was rationally designed and synthesized for differentiating cancer cells from normal cells owing to the existence of relatively high endogenous levels of both biomarkers in cancer cells.


The Analyst ◽  
2019 ◽  
Vol 144 (23) ◽  
pp. 6975-6980 ◽  
Author(s):  
Zilu Li ◽  
Chen Yu ◽  
Yanan Chen ◽  
Zihan Zhuang ◽  
Bin Tian ◽  
...  

A water-soluble fluorescent probe with ultra-sensitivity over a wider pH range was developed to differentiate cancer cells from normal cells.


Author(s):  
Fereshteh Mansoury ◽  
Soheila Abdi ◽  
Nahid Babaei ◽  
Maliheh Entezari ◽  
Abbas Doosti ◽  
...  

Background: In recent years, the relationship between cancer cells and electromagnetic radiation has received much attention. Objectives: The present study aimed to evaluate the effects of different intensities of electromagnetic fields on gastric cancer cell lines (AGS). Methods: After preparing AGS and Hu02 (normal) cell lines, they were exposed to magnetic flux densities of 0.25, 0.5, 1, and 2 millitesla (mT) for 18 h. The cell viability was studied by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The expression levels of hes1 and hsa-circ-0068530 RNAs were studied by the quantitative Real-time-PCR technique. Results: The inhibition of gastric cancer cell line growth was observed under the influence of electromagnetic fields at different intensities. However, they did not affect the viability of normal cells. A sharp increase in the expression of hes1 and hsa-circ-0068530 genes was observed in normal cells exposed to 2 mT electromagnetic fields. Conclusions: In general, it can be concluded that the effect of electromagnetic fields on gastric cancer cells depends on their intensity. Magnetic flux densities of 0.25 and 0.5 mT had anti-cancer effects and magnetic flux density of 2 mT showed carcinogenic effects.


2020 ◽  
Author(s):  
Chittipolu Ajaykumar

Doxorubicin is an anthracycline antibiotic extracted from the bacterium Streptomyces peucetius. Its cytotoxic effect produced by intercalating with DNA causing breakdown of DNA strand which causes cancer cell apoptosis. Despite being an effective anticancer agent it causes several crucial side effects like carditoxicity, neuropathy, hepatotoxicity, nephrotoxicity, alopecia, typhlitis, myelosuppression, neutropenia, anaemia, thrombocytopenia, nausea, and diarrhoea were caused mainly due to the inability to distinguish between cancer cells and normal cells. This chapter mainly focuses on doxorubicin’s side effects, current understanding of the molecular mechanisms, and management and preventive strategies of doxorubicin’s cardiotoxicity during the treatment of various type of cancer.


Author(s):  
Gregory R. Moe ◽  
Lindsay M. Steirer ◽  
Joshua A. Lee ◽  
Adarsha Shivakumar ◽  
Alejandro D. Bolanos

Abstract Background Polysialic acid (polySia) modifies six cell surface proteins in humans mainly during fetal development and some blood cells in adults. Two genes in humans, ST8SIA2 and ST8SIA4, code for polysialyltransferases that synthesize polySia. ST8SIA2 is highly expressed during fetal development and in cancer but not in adult normal human cells. ST8SIA4 is expressed in fetal and adult brain, spleen, thymus, and peripheral blood leukocytes and in cancer. We identified a derivative of polySia containing de-N-acetyl neuraminic acid residues (dPSA), which is expressed on the cell surface of human cancer cell lines and tumors but not normal cells. Methods dPSA-modified proteins in several human cancer cell lines and normal blood cells were identified using co-immunoprecipitation with anti-dPSA antibodies, mass spectroscopy and Western blot. RNAi and CRISPR were used to knockdown and knockout, respectively, the polysialyltransferase genes in human melanoma SK-MEL-28 and neuroblastoma CHP-134 cell lines, respectively, to determine the effect on production of cell surface dPSA measured by flow cytometry and fluorescence microscopy. Results We found that dPSA is linked to or associated with nucleolin, a nuclear protein reported to be on the cell surface of cancer but not normal cells. Knocking down expression of ST8SIA2 with RNAi or knocking out each gene individually and in combination using CRISPR showed that cell surface dPSA depended on expression of ST8SIA2. Conclusions The presence of dPSA specifically in a broad range of human cancers but not human adult normal cells offers novel possibilities for diagnosis, prevention and treatment targeting the dPSA antigen that appears to be cancer-specific, consistent across not only human cancers but also species, and may be an unrecognized mechanism of immune shielding.


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