Peiminine Enhances Doxorubicin Cytotoxicity and Downregulates hsa-miR-106a-5p and hsa -miR-181a-5p in Human Gastric Adenocarcinoma Cells

Background: Gastric cancer (GC) is a prevalent and deadly cancer worldwide. Chemotherapy is the primary treatment, but some patients use herbal remedies, such as Peiminine from Fritillaria walujewii, for palliative care. Cancer cells can affect the expression of noncoding RNAs, like microRNA, which...

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Main Authors: Shirin Hedayati, Hossein Soltanzadeh, Hadi Esmaeili Gouvarchin Ghaleh, Zahra Hojjati Bonab, Akbar Ghorbani Alvanegh
Format: Article
Language:English
Published: Wolters Kluwer Medknow Publications 2024-12-01
Series:Advanced Biomedical Research
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Online Access:https://journals.lww.com/10.4103/abr.abr_535_23
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author Shirin Hedayati
Hossein Soltanzadeh
Hadi Esmaeili Gouvarchin Ghaleh
Zahra Hojjati Bonab
Akbar Ghorbani Alvanegh
author_facet Shirin Hedayati
Hossein Soltanzadeh
Hadi Esmaeili Gouvarchin Ghaleh
Zahra Hojjati Bonab
Akbar Ghorbani Alvanegh
author_sort Shirin Hedayati
collection DOAJ
description Background: Gastric cancer (GC) is a prevalent and deadly cancer worldwide. Chemotherapy is the primary treatment, but some patients use herbal remedies, such as Peiminine from Fritillaria walujewii, for palliative care. Cancer cells can affect the expression of noncoding RNAs, like microRNA, which can then influence the expression of genes. This research aims to study the effects of Peiminine on Doxorubicin cytotoxicity and detect the expression levels of hsa-miR-106a-5p and hsa-miR-181a-5p in AGS human gastric adenocarcinoma cells. Materials and Methods: AGS cells were cultured and treated with different concentrations of Peiminine. An MTT assay was performed to determine the concentration of Peiminine required to prohibit 50% cell growth (IC50) and the cell viability percentage of the AGS cell line. The percentage of AGS cell line apoptosis was determined using acridine orange (AO) and ethidium bromide (EtBr). Finally, molecular studies were conducted to compare hsa-miR-106a-5p and hsa-miR-181a-5p expression in the control and treated groups. Results: According to the study, Peiminine has been found to enhance the cytotoxicity of Doxorubicin, which reduces cell viability and increases apoptosis in the AGS cell line. Furthermore, the study also indicates that the AGS cell line treated with Peiminine shows lower expression of hsa -miR-106a-5p and hsa -miR-181a-5p compared to the control group that was not treated. Conclusion: Peiminine enhances Doxorubicin’s effectiveness, inhibits AGS cell line growth, and reduces miRNA expression. Further research is needed for potential use as a supplementary GC treatment.
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spelling doaj-art-0aeeb3a1e748440b83f67c2423a7d3202025-01-08T13:16:00ZengWolters Kluwer Medknow PublicationsAdvanced Biomedical Research2277-91752024-12-0113112112110.4103/abr.abr_535_23Peiminine Enhances Doxorubicin Cytotoxicity and Downregulates hsa-miR-106a-5p and hsa -miR-181a-5p in Human Gastric Adenocarcinoma CellsShirin HedayatiHossein SoltanzadehHadi Esmaeili Gouvarchin GhalehZahra Hojjati BonabAkbar Ghorbani AlvaneghBackground: Gastric cancer (GC) is a prevalent and deadly cancer worldwide. Chemotherapy is the primary treatment, but some patients use herbal remedies, such as Peiminine from Fritillaria walujewii, for palliative care. Cancer cells can affect the expression of noncoding RNAs, like microRNA, which can then influence the expression of genes. This research aims to study the effects of Peiminine on Doxorubicin cytotoxicity and detect the expression levels of hsa-miR-106a-5p and hsa-miR-181a-5p in AGS human gastric adenocarcinoma cells. Materials and Methods: AGS cells were cultured and treated with different concentrations of Peiminine. An MTT assay was performed to determine the concentration of Peiminine required to prohibit 50% cell growth (IC50) and the cell viability percentage of the AGS cell line. The percentage of AGS cell line apoptosis was determined using acridine orange (AO) and ethidium bromide (EtBr). Finally, molecular studies were conducted to compare hsa-miR-106a-5p and hsa-miR-181a-5p expression in the control and treated groups. Results: According to the study, Peiminine has been found to enhance the cytotoxicity of Doxorubicin, which reduces cell viability and increases apoptosis in the AGS cell line. Furthermore, the study also indicates that the AGS cell line treated with Peiminine shows lower expression of hsa -miR-106a-5p and hsa -miR-181a-5p compared to the control group that was not treated. Conclusion: Peiminine enhances Doxorubicin’s effectiveness, inhibits AGS cell line growth, and reduces miRNA expression. Further research is needed for potential use as a supplementary GC treatment.https://journals.lww.com/10.4103/abr.abr_535_23doxorubicingastric cancermicrornas
spellingShingle Shirin Hedayati
Hossein Soltanzadeh
Hadi Esmaeili Gouvarchin Ghaleh
Zahra Hojjati Bonab
Akbar Ghorbani Alvanegh
Peiminine Enhances Doxorubicin Cytotoxicity and Downregulates hsa-miR-106a-5p and hsa -miR-181a-5p in Human Gastric Adenocarcinoma Cells
Advanced Biomedical Research
doxorubicin
gastric cancer
micrornas
title Peiminine Enhances Doxorubicin Cytotoxicity and Downregulates hsa-miR-106a-5p and hsa -miR-181a-5p in Human Gastric Adenocarcinoma Cells
title_full Peiminine Enhances Doxorubicin Cytotoxicity and Downregulates hsa-miR-106a-5p and hsa -miR-181a-5p in Human Gastric Adenocarcinoma Cells
title_fullStr Peiminine Enhances Doxorubicin Cytotoxicity and Downregulates hsa-miR-106a-5p and hsa -miR-181a-5p in Human Gastric Adenocarcinoma Cells
title_full_unstemmed Peiminine Enhances Doxorubicin Cytotoxicity and Downregulates hsa-miR-106a-5p and hsa -miR-181a-5p in Human Gastric Adenocarcinoma Cells
title_short Peiminine Enhances Doxorubicin Cytotoxicity and Downregulates hsa-miR-106a-5p and hsa -miR-181a-5p in Human Gastric Adenocarcinoma Cells
title_sort peiminine enhances doxorubicin cytotoxicity and downregulates hsa mir 106a 5p and hsa mir 181a 5p in human gastric adenocarcinoma cells
topic doxorubicin
gastric cancer
micrornas
url https://journals.lww.com/10.4103/abr.abr_535_23
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