Cladosporol A triggers apoptosis sensitivity by ROS-mediated autophagic flux in human breast cancer cells

Koul, Mytre; Kumar, Ashok; Deshidi, Ramesh; Sharma, Vishal; Singh, Rachna D.; Singh, Jasvinder; Sharma, Parduman R.; Shah, Bhahwal Ali; Jaglan, Sundeep; Singh, Shashank

doi:10.1186/s12860-017-0141-0

Cited by 31 publications

(32 citation statements)

References 37 publications

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“…Our results are in agreement with those of recently published studies that demonstrated the correlation between oxidative stress, the production of ROS, and the induction of apoptosis. 45,46 It has been revealed that the ROS induction pathway can be beneficial for developing therapeutic perspectives of cancer. 46,47 There are a few reports which reported the role of ribonuclease and/or its modified form in the ROS production and apoptosis induction.…”

Section: Discussionmentioning

confidence: 99%

PEGylated gold nanoparticles-ribonuclease induced oxidative stress and apoptosis in colorectal cancer cells

et al. 2019

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Introduction: Currently, drug-induced reactive oxygen species (ROS) mediating apoptosis pathway have extensively been investigated in designing effective strategies for colorectal cancer (CRC) chemotherapy. Bovine pancreatic ribonuclease A (RNase A) represents a new class of cytotoxic and non-mutagenic enzymes, and has gained more attention as a potential anticancer modality; however, the cytosolic ribonuclease inhibitors (RIs) restrict the clinical application of this enzyme. Nowadays, nanotechnology-based diagnostic and therapeutic systems have provided potential solutions for cancer treatments. Methods: In this study, the gold nanoparticles (AuNPs) were synthesized, stabilized by polyethylene glycol (PEG), functionalized, and covalently conjugated with RNase A. The physicochemical properties of engineered nanobiomedicine (AuNPs-PEG-RNase A) were characterized by scanning electron microscope (SEM), dynamic light scattering (DLS), and UV-vis spectrum. Then, its biological impacts including cell viability, apoptosis, and ROS production were evaluated in the SW-480 cells. Results: The engineered nanobiomedicine, AuNPs-PEG-RNase A, was found to effectively induce apoptosis in SW-480 cells and result in a significant reduction in cancer cell viability. Besides, the maximum production of ROS was obtained after the treatment of cells with an IC50 dose of AuNPs-PEG-RNase A. Conclusion: Based on the efficient ROS-responsiveness and the anticancer activity of RNase A of the engineered nanomedicine, this nanoscaled biologics may be considered as a potential candidate for the treatment of CRC.

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Section: Discussionmentioning

confidence: 99%

PEGylated gold nanoparticles-ribonuclease induced oxidative stress and apoptosis in colorectal cancer cells

et al. 2019

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“…Herein, results indicated that UA increased the levels of Ca 2+ with 12-48 h treatment, and reduced Ψ m at 48 h, however, it did not significantly affect the production of ROS by NCI-H292 cells. Literature reports that the production of ROS is involved in apoptotic cell death (38). However, we suggest that UA-induced cell apoptosis is independent of ROS pathways.…”

Section: Discussionmentioning

confidence: 52%

Ursolic Acid Induces Apoptotic Cell Death Through AIF and Endo G Release Through a Mitochondria-dependent Pathway in NCI-H292 Human Lung Cancer Cells In Vitro

Chen

Shih

Yeh

et al. 2019

In Vivo

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Background/Aim: Ursolic acid (UA), a triterpene compound present in natural plants, has been shown to induce cytotoxic effects on many human cancer cells through induction of cell-cycle arrest and apoptosis. This study investigated the effects of UA on human lung cancer NCI-H292 cells in vitro. Materials and Methods: Flow cytometric assay was used to measure the percentage of cell viability, apoptotic cell death by double staining of annexin V and propidium iodide (PI), production of reactive oxygen species (ROS) and Ca 2+ , and mitochondriaI membrane potential (Ψ m). UA-induced chromatin condensation and DNA fragmentation were examined by 4',6-diamidino-2-phenylindole staining and DNA gel electrophoresis, respectively. Western blotting was used to examine the changes of apoptosis-associated protein expression in NCI-H292 cells. Results: UA reduced cell viability and induced apoptotic cell death. UA increased Ca 2+ production, reduced Ψ m , but did not affect ROS production in NCI-H292 cells. UA increased apoptosis-inducing factor (AIF) and endonuclease G in NCI-H292 cells. Conclusion: Based on these observations, we suggest UA induces apoptotic cell death via AIF and Endo G release through a mitochondria-dependent pathway in NCI-H292 cells. Lung cancer is the leading cause of cancer-associated death worldwide (1) and divided into non-small-cell lung cancer (NSCLC) and small-cell lung cancer (SCLC). The most common type is NSCLC accounting for about 80-85% (2, 3), with poor prognosis and a high incidence of recurrence (4). NSCLC includes adenocarcinoma, squamous cell carcinoma, and large-cell carcinomas (5). Although advanced diagnostics and therapeutics have been developed, the treatment and outcome of lung cancer is still unsatisfactory (4, 6-8). Characteristics of cancer include uncontrolled cell-cycle progression and deregulation of apoptosis. One of the therapeutic strategies for chemotherapy is to induce cancer cell apoptosis. Apoptosis plays a critical role in the balance between cellular replication and death, in particular for elimination of unwanted, damaged or infected cells (9, 10). Much evidence has shown that chemotherapy drugs in clinical used for patients with cancer via the activation of apoptotic pathways in cancer cells (11-13). When the mitochondria membrane potential (Ψ m) decreases, cytochrome c binds to 383 This article is freely accessible online.

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“…Seo, Kim, Dhanasekaran, Tsang, and Song () have used confocal microscopy to show apoptosis in curcumin‐treated ovarian cancer (PA1, MDAH 2774 and SKOV3) cells by analyzing cytosolic Ca 2+ concentrations. Laser scanning confocal microscopy has been used to measure the mitochondrial transmembrane potential to confirm apoptosis in Cladosporol A, a phytochemical isolated from Cladosporium cladosporioides , treated MCF‐7 cells by Koul et al ().…”

Section: Detection Of Apoptosismentioning

confidence: 99%

In vitro assays and techniques utilized in anticancer drug discovery

Ediriweera

Tennekoon

Samarakoon

2018

J of Applied Toxicology

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Development of a cancer is a multistep process and six major hallmarks of cancer that are known to control malignant transformation have been described. Anticancer drug development is a tedious process, requiring a number of in vitro, in vivo and clinical studies. In vitro assays provide an initial platform for cancer drug discovery approaches. A wide range of in vitro assays/techniques have been developed to evaluate each hallmark feature of cancer and selection of a particular in vitro assay or technique mainly depends on the specific research question (s) to be examined. In the present review, we have described some commonly utilized in vitro assays and techniques used to examine cell viability/proliferation, apoptosis, cellular senescence, invasion and migration, oxidative stress and antioxidant effects, gene and protein expression, angiogenesis and genomic alterations in cancer drug discovery. Additionally, uses of modern techniques such as high throughput screening, high content screening and reporter gene assays in cancer drug discovery have also been described.

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Cladosporol A triggers apoptosis sensitivity by ROS-mediated autophagic flux in human breast cancer cells

Cited by 31 publications

References 37 publications

PEGylated gold nanoparticles-ribonuclease induced oxidative stress and apoptosis in colorectal cancer cells

PEGylated gold nanoparticles-ribonuclease induced oxidative stress and apoptosis in colorectal cancer cells

Ursolic Acid Induces Apoptotic Cell Death Through AIF and Endo G Release Through a Mitochondria-dependent Pathway in NCI-H292 Human Lung Cancer Cells In Vitro

In vitro assays and techniques utilized in anticancer drug discovery

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