Retinoic Acid Treatment of Human Hematological Malignancies Induces Caspase Dependent and Independent Apoptotic Cell Death
DOI:
https://doi.org/10.37506/ijfmt.v15i1.13598Keywords:
Retinoic Acid, SR, NB4, THP1, COLO677, ApoptosisAbstract
The unprejudiced of this education is to gauge the ability of the retinoic acid to induce apoptotic cell death
in hematological tumors through caspase dependent or independent apoptotic pathway, The cytotoxicity
effects of retinoic acid of different concentrations (400,350,300,250,200,150,100,50,25,12.5 µg\ml) and
exposure for all hematological malignancy cell lines (Human non-Hodgkin lymphoma SR and human
multiple myeloma (COLO 677) and Human Monocytic Leukemia THP1 and Acute promyelocytic leukemia
NB4) have been determined using a microtetrazolium (MTT) assay. Propodeum iodide and alcidine orange
(AO/PI) paired discoloration was used to study the ability of retinoic acid to induce apoptosis in the infected
cells and examined under fluorescence microscope and quantified for the percentage of apoptosis induction.
Quantitative immunocytochemistry assay was used to study the caspase dependent and independent
proteins expression in infected and control cells. Cells treated with Retinoic Acid showed increased cell
death percentage compared to the untreated cells as quantified by MTT assay. AO/PI results revealed that
Retinoic Acid had powerful effect on inducing apoptosis significantly (p<0.001) in human cancer cell lines
tested, compared to control cell. Immunocytochemistry in Retinoic Acid infected human hematological cell
lines revealed remarkable increase in expression of caspase 8,9 (dependent pathway) and AIF, ENDOG
(independent pathway) induces a significant (p<0.002) as compared untreated cell.
This study, which shows the role of the Retinoic Acid in inducing apoptosis through a dependent and
independent pathway in cancer cells, we anticipation these annotations will shanty light on the impending
exploration of retinoic acid in cancer hindrance and rehabilitation
Published
How to Cite
Issue
Section

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
Re use and mixing of content policy- We follow Creative Commons Licence Policy. We follow CC BY. Please refer below for all details
https://creativecommons.org/licenses/
CC BY
This license lets others distribute, remix, adapt, and build upon our work, even commercially, as long as they credit us for the original creation.
- The journal allows readers to read, download, copy, distribute, print, search, or link to the full texts of its articles and allow readers to use them for any other lawful purpose.
- The journal allows the author(s) to hold the copyright without restrictions.
- The journal allows the author(s) to retain publishing rights without restrictions