Molecular mechanism of apoptosis induction by Gaillardin, a sesquiterpene lactone, in breast cancer cell lines

Fallahian, Faranak; Aghaei, Mahmoud; Abdolmohammadi, Mohammad Hossein; Hamzeloo-Moghadam, Maryam

doi:10.1007/s10565-016-9312-6

Cited by 31 publications

(28 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Wei et al [33] found that miR-497-mediated BCL-2 degradation resulted in suppressed proliferation of breast cancer cells. Similar results were observed in research carried out by Fallahian et al [34] and Li et al [35] found that BCL-2 downregulation increased apoptosis in breast cancer cells. Hence, we found BCL-2 to be an attractive target for further research.…”

Section: Discussionsupporting

confidence: 91%

MicroRNA-148a promotes apoptosis and suppresses growth of breast cancer cells by targeting B-cell lymphoma 2

Ren

Shi

et al. 2017

Anti-Cancer Drugs

View full text Add to dashboard Cite

MicroRNAs (miRNAs) contribute toward tumorigenesis through the modulation of tumor-related genes. MiR-148a has been characterized as a tumor-suppressing miRNA and its downregulation has been reported in tumors of a variety of cancers. However, the functional role of miR-148a in breast cancer is not yet fully understood. Using both in-vitro and in-vivo models, we confirmed that miR-148a acts to inhibit the proliferation of breast cancer cells. Through the use of bioinformatic approaches in miRNA target prediction, we determined that B-cell lymphoma 2 (BCL-2) is a likely target of miR-148a. The overexpression and tumorigenic effects of BCL-2 have already been confirmed in cancerous tumors of the breast. A dual-luciferase assay was performed to confirm that miR-148a targets the 3'-untranslated region of BCL-2. In this study, we first characterized the downregulation of miR-148a in breast cancer tissues. We then found that restoring expression of miR-148a suppressed the expression of BCL-2 at the level of both mRNA and protein. Upregulation of miR-148a caused a subsequent reduction of proliferation and an increase in apoptosis. In conclusion, we have confirmed the role of miR-148a as a pivotal regulator in breast cancer through its targeting of BCL-2. This evidence strongly suggests that miR-148a could prove to be a novel therapeutic target in breast cancer.

show abstract

Section: Discussionsupporting

confidence: 91%

MicroRNA-148a promotes apoptosis and suppresses growth of breast cancer cells by targeting B-cell lymphoma 2

Ren

Shi

et al. 2017

Anti-Cancer Drugs

View full text Add to dashboard Cite

show abstract

“…31,32) ROS participates in P53-mediated mitochondrial apoptosis through regulating mitochondrial membrane potential and inducing Cyto C release and activation of caspase cascades. [33][34][35] In addition to ROS, P53 could activate mitochondrial pathway through regulation of Bax and Bcl-2 family members. [36][37][38] The results in the current study showed that downregulation of miR-30 promoted ROS generation through activation of P53.…”

Section: Discussionmentioning

confidence: 99%

miR-30 functions as an oncomiR in gastric cancer cells through regulation of P53-mediated mitochondrial apoptotic pathway

Wang

Jiao

Cui

et al. 2017

Bioscience, Biotechnology, and Biochemistry

View full text Add to dashboard Cite

The present study was designed to investigate the role of miR-30 in the development of Gastric cancer (GC). miR-30 expression was increased in GC tissues and cell lines. Downregulation of miR-30 inhibited cell proliferation and promoted apoptosis in HGC-27 cells. Upregulation of miR-30 enhanced the proliferation and inhibited apoptosis. P53 expression was decreased in GC tissues. P53 expression was correlated with miR-30 expression. Downregulation of miR-30 increased P53 expression. Knockdown of P53 inhibited miR-30-inhibitor-induced suppression of cell proliferation and increase of apoptosis. Downregulation of miR-30 increased ROS generation which was inhibited by shP53. miR-30 inhibitors induced a decrease in mitochondrial oxygen consumption, cytoplasmic release of cytochrome c, and activation of Caspase 3 and 9, activating mitochondrial apoptotic pathway. Downregulation of P53 and N-acetyl-cysteine suppressed miR-30 inhibitors-activated mitochondrial dysfunction and apoptotic events. In conclusion, we identified that miR-30 functioned as a potential oncomiR through P53/ROS-mediated regulation of mitochondrial apoptotic pathway.

show abstract

“…At least 10,000 cells were analyzed for each sample. The apoptosis rate was calculated using the following formula 14 : Apoptosis rate (%)=(Number of apoptotic cells/Number of total cells observed)×100.…”

Section: Methodsmentioning

confidence: 99%

Euphorbia factor L2 induces apoptosis in A549 cells through the mitochondrial pathway

Lin

Tang

Zhang

et al. 2017

Acta Pharmaceutica Sinica B

View full text Add to dashboard Cite

Euphorbia factor L2, a lathyrane diterpenoid isolated from caper euphorbia seed (the seeds of Euphorbia lathyris L.), has been traditionally applied to treat cancer. This article focuses on the cytotoxic activity of Euphorbia factor L2 against lung carcinoma A549 cells and the mechanism by which apoptosis is induced. We analyzed the cytotoxicity and related mechanism of Euphorbia factor L2 with an MTT assay, an annexin V-FITC/PI test, a colorimetric assay, and immunoblotting. Euphorbia factor L2 showed potent cytotoxicity to A549 cells. Euphorbia factor L2 led to an increase in reactive oxygen species (ROS) generation, a loss of mitochondrial electrochemical potential, release of cytochrome c, activation of caspase-9 and caspase-3, and cleavage of poly(ADP-ribose) polymerase, suggesting that Euphorbia factor L2 induced apoptosis through a mitochondrial pathway. The cytotoxic activity of Euphorbia factor L2 in A549 cells and the related mechanisms of apoptotic induction provide support for the further investigation of caper euphorbia seeds.

show abstract

Molecular mechanism of apoptosis induction by Gaillardin, a sesquiterpene lactone, in breast cancer cell lines

Cited by 31 publications

References 28 publications

MicroRNA-148a promotes apoptosis and suppresses growth of breast cancer cells by targeting B-cell lymphoma 2

MicroRNA-148a promotes apoptosis and suppresses growth of breast cancer cells by targeting B-cell lymphoma 2

miR-30 functions as an oncomiR in gastric cancer cells through regulation of P53-mediated mitochondrial apoptotic pathway

Euphorbia factor L2 induces apoptosis in A549 cells through the mitochondrial pathway

Contact Info

Product

Resources

About