Spiroquinazolinone-induced cytotoxicity and apoptosis in K562 human leukemia cells: alteration in expression levels of Bcl-2 and Bax

Ghasemian, Majid; Mahdavi, Majid; Zare, Payman; Feizi, Mohammad Ali Hosseinpour

doi:10.2131/jts.40.115

Cited by 43 publications

(13 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Studies have shown that the death receptor pathway of the mitochondrial pathway is a classic pathway of apoptosis in many tumor cells (16). Bcl-2 and Bax play a key role in the mitochondrial apoptotic pathway (17). In many tumors, including lung cancer, the expression of Bcl-2 is increased in tumors and Bax is decreased (18).…”

Section: Discussionmentioning

confidence: 99%

Upregulation of the Kank1 gene inhibits human lung cancer progression in�vitro and in�vivo

Zhang

2018

Oncol Rep

View full text Add to dashboard Cite

Kank1, an important member of the Kank gene family, plays an important role in the development of many malignant tumors. As a brand new tumor-suppressor gene, the expression of Kank1 gene has been revealed to be downregulated or absent in many malignant tumors. However, there is no study concerning the specific role of Kank1 in the development and progression of lung cancer. In the present study, we found that the Kankl gene was significantly downregulated in human lung cancer and lung cancer cells. When the Kankl gene was upregulated, we found that the proliferation of lung cancer cells was significantly inhibited, the cells were arrested in the G0/G1 phase, the apoptosis of cells was observed, the expression of the caspase family of genes was altered with mainly the activation of caspase-3 and -9, and Bcl-2/Bax ratio was significantly imbalanced. In addition, we also found that upregulation of the Kankl gene resulted in the inhibition of tumor cell invasion and metastasis. Concurrently, in vivo nude mice experiments also confirmed that upregulation of Kank1 expression led to reduced tumor formation in nude mice and significantly reduced tumor volume. These results revealed that upregulation of the Kankl gene inhibited the progression of lung cancer both in vitro and in vivo, and its mechanism was closely related to cell apoptosis as well as tumor invasion and metastasis.

show abstract

Section: Discussionmentioning

confidence: 99%

Upregulation of the Kank1 gene inhibits human lung cancer progression in�vitro and in�vivo

Zhang

2018

Oncol Rep

View full text Add to dashboard Cite

show abstract

“…Most chemotherapeutic drugs act via stimulating apoptosis of cancer cells. However, toxicity and resistance lead to failure of chemotherapy in CML patients (Ghasemian et al, 2015). For that reason, natural compounds are increasingly considered alternative treatment that has potentials for therapy.…”

Section: Introductionmentioning

confidence: 99%

Jellyfish extract induces apoptotic cell death through the p38 pathway and cell cycle arrest in chronic myelogenous leukemia K562 cells

Jin

Kwak

et al. 2017

PeerJ

View full text Add to dashboard Cite

Jellyfish species are widely distributed in the world’s oceans, and their population is rapidly increasing. Jellyfish extracts have several biological functions, such as cytotoxic, anti-microbial, and antioxidant activities in cells and organisms. However, the anti-cancer effect of Jellyfish extract has not yet been examined. We used chronic myelogenous leukemia K562 cells to evaluate the mechanisms of anti-cancer activity of hexane extracts from Nomura’s jellyfish in vitro. In this study, jellyfish are subjected to hexane extraction, and the extract is shown to have an anticancer effect on chronic myelogenous leukemia K562 cells. Interestingly, the present results show that jellyfish hexane extract (Jellyfish-HE) induces apoptosis in a dose- and time-dependent manner. To identify the mechanism(s) underlying Jellyfish-HE-induced apoptosis in K562 cells, we examined the effects of Jellyfish-HE on activation of caspase and mitogen-activated protein kinases (MAPKs), which are responsible for cell cycle progression. Induction of apoptosis by Jellyfish-HE occurred through the activation of caspases-3,-8 and -9 and phosphorylation of p38. Jellyfish-HE-induced apoptosis was blocked by a caspase inhibitor, Z-VAD. Moreover, during apoptosis in K562 cells, p38 MAPK was inhibited by pretreatment with SB203580, an inhibitor of p38. SB203580 blocked jellyfish-HE-induced apoptosis. Additionally, Jellyfish-HE markedly arrests the cell cycle in the G0/G1 phase. Therefore, taken together, the results imply that the anti-cancer activity of Jellyfish-HE may be mediated apoptosis by induction of caspases and activation of MAPK, especially phosphorylation of p38, and cell cycle arrest at the Go/G1 phase in K562 cells.

show abstract

“…In our present study, the expressions of cleaved caspase-7 and -8 were significantly increased by tanshinone IIA, but there was no change in that of cleaved caspase-9 (Figure 4). Two major molecular pathways that trigger programmed cell death are the caspase-mediated intrinsic pathway, which is induced by cellular stresses, and the extrinsic pathway, which is related to the death receptor [25]. Both pathways activate the apoptotic caspases, resulting in morphological and biochemical cellular alterations related to apoptosis [26].…”

Section: Resultsmentioning

confidence: 99%

Analysis and Identification of Active Compounds from Salviae miltiorrhizae Radix Toxic to HCT-116 Human Colon Cancer Cells

et al. 2020

View full text Add to dashboard Cite

Colorectal cancer is one of the most frequently diagnosed cancers worldwide. The aim of the present study was to simultaneously analyze compounds of Salviae miltiorrhizae Radix (SMR) and determine their cytotoxic effects on HCT-116 human colorectal cancer cells. We established a simultaneous analysis method of five compounds (salvianic acid A, salvianolic acid B, caffeic acid, tanshinone IIA, and rosmarinic acid) contained in SMR, and found that among the various compounds in SMR, tanshinone IIA significantly decreased cell viability in a concentration-dependent manner. Hoechst staining also showed that both SMR and tanshinone IIA increased nuclear condensation, suggesting induction of apoptosis. By Western blotting, we found that tanshinone IIA induced apoptotic cell death, significantly increased Bax, but decreased Bcl-2 in the course of apoptosis. Tanshinone IIA increased the expression of cleaved caspases-7 and -8. Tanshinone IIA was shown to be an active ingredient of SMR that may be a useful chemotherapeutic strategy for patients with colorectal cancer.

show abstract

Spiroquinazolinone-induced cytotoxicity and apoptosis in K562 human leukemia cells: alteration in expression levels of Bcl-2 and Bax

Cited by 43 publications

References 38 publications

Upregulation of the Kank1 gene inhibits human lung cancer progression in�vitro and in�vivo

Upregulation of the Kank1 gene inhibits human lung cancer progression in�vitro and in�vivo

Jellyfish extract induces apoptotic cell death through the p38 pathway and cell cycle arrest in chronic myelogenous leukemia K562 cells

Analysis and Identification of Active Compounds from Salviae miltiorrhizae Radix Toxic to HCT-116 Human Colon Cancer Cells

Contact Info

Product

Resources

About