Summary of Study ST002755

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001716. The data can be accessed directly via it's Project DOI: 10.21228/M8WM6F This work is supported by NIH grant, U2C- DK119886.

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This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST002755
Study TitleMetabolomics Profiling of the Antiproliferative, Anti-migratory and Anti-invasive Potential of Amlodipine in Lung Cancer Cells
Study TypeLC/MS/MS
Study SummaryLung cancer is still among the most leading causes of cancer-related deaths across the world. Although chemotherapy is considered as a critical choice to manage/limit cancer growth in lung cancer patients with early-stage and advanced cancer stages, it has many limitations including, at least, the severe side effects and chemoresistance. The latter is one of the considerable challenges to lung cancer treatment. Therefore, identification of new alternative therapies with lesser cytotoxic effects when compared to the currently used chemotherapeutics is one of the current research approaches. Calcium channel blockers (CCBs) are emerging as anti-cancer agents in several cancer types. Our objective is to determine the cytotoxic effect of amlodipine on non-small cell lung cancer (NSCLC) cells. Colorimetric MTT cell proliferation assay was used to analyze cell viability following treatments with amlodipine in A549 and H1299 NSCLC cell lines. ANOVA and Tukey’s multiple comparison test were used to detect statistical significance. Half maximal (50%) inhibitory concentration (IC50) values were obtained by applying nonlinear regression curve fit analysis. To assess the effect of amlodipine on A549 and H1299 NSCLC cells migration and invasion scratch wound-healing assay and cell invasion assay were used. Our study revealed that amlodipine significantly reduced proliferation of cancer cells in a dose-dependent fashion with half maximal (50%) inhibitory concentration (IC50) values of 23 and 25.66 µM in A549 and H1299 cells, respectively. Furthermore, amlodipine was able to reduce the invasiveness and migration of cancer cells, both of which are hallmarks in the pathogenesis of cancer, in both cell lines in a dose-dependent manner. Accordingly, our study provides empirical evidence that amlodipine expresses anti-cancer effect to NSCLC cells. However, additional investigations are required to further confirm our results on a larger scale at the clinical level.
Institute
Sharjah Institute for Medical Research
Last NameFacility
First NameCore
AddressM32, SIMR, College of Pharmacy, Health Sciences, University of Sharjah
Emailtims-tof@sharjah.ac.ae
Phone065057656
Submit Date2023-06-22
Raw Data AvailableYes
Raw Data File Type(s)d
Analysis Type DetailLC-MS
Release Date2023-07-18
Release Version1
Core Facility Core Facility
https://dx.doi.org/10.21228/M8WM6F
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Sample Preparation:

Sampleprep ID:SP002868
Sampleprep Summary:we used chloroform/methanol extraction protocol to increase the coverage of the extracted metabolites. At first, the samples (cells and buffer) were transferred into Eppendorf tubes then centrifuged at 14000 rpm for 5 minutes. Afterward, the buffer was discarded, and the cells were preserved. To each sample, 400 µL of the mixture containing one protease inhibitor tablet and 10 mL of lysis buffer was added. Following rest for 10 minutes, samples were transferred to 10 mL tubes, vortexed for 2–4 minutes, and sonicated with a COPLEY probe-sonicator (QSONICA SONICATOR, USA) for 30 seconds while utilizing a 30% amplifier in an ice bath. The samples were then transferred to Eppendorf tubes and centrifuged for 5 minutes at 14000 rpm. The supernatant was then transferred to another Eppendorf, and 400 µL of methanol and 300 µL of chloroform were added. Following that, the samples were vortexed for 30 seconds and centrifuged for 5 minutes at 14000 rpm. After that, two metabolite-containing layers are obtained, after transferring the upper layer of each sample to glass vials, 400 µl of methanol was added, followed by vertexing and centrifugation. The remaining supernatant was transferred to the same glass vials used before for the drying step, with the remaining protein pellets being air-dried for proteomics. A dried metabolomics sample was resuspended in 200 µL (0.1% formic acid in water) and injected into HPLC to be analysed by Q-TOF MS.
Extract Storage:-80℃
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