Apoptosis Detection Methods in Diagnosis of Cancer and Their Potential Role in Treatment: Advantages and Disadvantages: a Review

Khodavirdipour, Amir; Piri, Motahareh; Jabbari, Sarvin; Keshavarzi, Shiva; Safaralizadeh, Reza; Alikhani, Mohammad Yousef

doi:10.1007/s12029-020-00576-9

Cited by 16 publications

(11 citation statements)

References 71 publications

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“…Apoptosis is a programmed cellular process that occurs under either physiological or pathological conditions ( 41 ). Apoptosis exerts a vital role in the treatment of cancer, and induction of apoptosis is the eventual aim of numerous cancer therapies ( 42 ). The findings of the present study displayed that LCA induced apoptosis in LSCC cells and upregulated the level of cleaved caspase-3, cleaved PARP1 and Bax, meanwhile, LCA downregulated the level of Bcl-2.…”

Section: Discussionmentioning

confidence: 99%

Licochalcone A induces cell cycle arrest and apoptosis via suppressing MAPK signaling pathway and the expression of FBXO5 in lung squamous cell cancer

Fan,

Guan,

Wang

et al. 2023

Oncol Rep

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Lung squamous cell carcinoma (LSCC) is a highly heterogeneous malignancy with high mortality and few therapeutic options. Licochalcone A (LCA, PubChem ID: 5318998) is a chalcone extracted from licorice and possesses anticancer and anti-inflammatory activities. The present study aimed to elucidate the anticancer effect of LCA on LSCC and explore the conceivable molecular mechanism. MTT assay revealed that LCA significantly inhibited the proliferation of LSCC cells with less cytotoxicity towards human bronchial epithelial cells. 5-ethynyl-2′-deoxyuridine (EdU) assay demonstrated that LCA could reduce the proliferation rate of LSCC cells. The flow cytometric assays indicated that LCA increased the cell number of the G1 phase and induced the apoptosis of LSCC cells. LCA downregulated the protein expression of cyclin D1, cyclin E, CDK2 and CDK4. Meanwhile, LCA increased the expression level of Bax, cleaved poly(ADP-ribose)polymerase-1 (PARP1) and caspase 3, as well as downregulated the level of Bcl-2. Proteomics assay demonstrated that LCA exerted its antitumor effects via inhibiting mitogen-activated protein kinase (MAPK) signaling pathways and the expression of F-box protein 5 (FBXO5). Western blot analysis showed that LCA decreased the expression of p-ERK1/2, p-p38MAPK and FBXO5. In the xenograft tumors of LSCC, LCA significantly inhibited the volumes and weight of tumors in nude mice with little toxicity in vital organs. Therefore, the present study demonstrated that LCA effectively inhibited cell proliferation and induced apoptosis in vitro , and suppressed xenograft tumor growth in vivo . LCA may serve as a future therapeutic candidate of LSCC.

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Section: Discussionmentioning

confidence: 99%

Licochalcone A induces cell cycle arrest and apoptosis via suppressing MAPK signaling pathway and the expression of FBXO5 in lung squamous cell cancer

Fan,

Guan,

Wang

et al. 2023

Oncol Rep

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“…After further incubation with 3,3-diaminobenzidine (DAB) for 10 min. Light microscopy was used to observe the immunized proteins ( 18 , 19 ).…”

Section: Methodsmentioning

confidence: 99%

Chronic exposure to yttrium induced cell apoptosis in the testis by mediating Ca2+/IP3R1/CaMKII signaling

Liu

Ding

Xie

et al. 2023

Front. Public Health

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IntroductionEnvironmental pollutants, such as rare earth elements, affect human health and particularly induce reproductive system injury. Yttrium (Y), one of the most widely used heavy rare earth elements, has been reported the cytotoxicity. However, the biological effects of Y3+ in the human body are largely unknown.MethodsTo further investigate the effects of Y on the reproductive system, in vivo (rat models) and in vitro studies were performed. Histopathological and immunohistochemical examination were conducted, and western blotting assays were performed to detect the protein expression. TUNEL/DAPI staining were used to detect cell apoptosis, and the intracellular calcium concentrations were also determined.ResultsLong-term exposure to YCl3 in rats produced significant pathological changes. YCl3 treatment could induce cell apoptosis in vivo and in vitro. In addition, YCl3 enhanced the concentration of cytosolic Ca2+ and up regulated the expression of IP3R1/CaMKII axis in Leydig cells. However, inhibition of IP3R1 and CaMKII with 2-APB and KN93, respectively, could reverse these effects.ConclusionLong-term exposure to yttrium could induce testicular injury by stimulating cell apoptosis, which might be associated with activation of Ca2+/IP3R1/CaMKII axis in Leydig cells.

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“…NCI-H460 cells were seeded following the same procedure used for determining the mitotic index. After 24 h of treatment with the test compounds, both the cells suspended in the medium, and those attached to the plate surface were gathered and subjected to processing using the "Annexin V-FITC Apoptosis Detection Kit" (eBioscience, Vienna, Austria) [46,47] according to the manufacturer's instructions. Apoptosis rates were determined by flow cytometry (BD Accuri™ C6 Plus Flow cytometer, BD Biosciences, Qume Drive, San Jose, CA, USA), and data were analyzed using BD Accuri TM C6 Plus software version 1.0.27.1 At least 20,000 events per sample were collected.…”

Section: Apoptosis Analysismentioning

confidence: 99%

BP-M345 as a Basis for the Discovery of New Diarylpentanoids with Promising Antimitotic Activity

Moreira,

Silva,

Castro

et al. 2024

IJMS

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Recently, the diarylpentanoid BP-M345 (5) has been identified as a potent in vitro growth inhibitor of cancer cells, with a GI50 value between 0.17 and 0.45 µM, showing low toxicity in non-tumor cells. BP-M345 (5) promotes mitotic arrest by interfering with mitotic spindle assembly, leading to apoptotic cell death. Following on from our previous work, we designed and synthesized a library of BP-M345 (5) analogs and evaluated the cell growth inhibitory activity of three human cancer cell lines within this library in order to perform structure–activity relationship (SAR) studies and to obtain compounds with improved antimitotic effects. Four compounds (7, 9, 13, and 16) were active, and the growth inhibition effects of compounds 7, 13, and 16 were associated with a pronounced arrest in mitosis. These compounds exhibited a similar or even higher mitotic index than BP-M345 (5), with compound 13 displaying the highest antimitotic activity, associated with the interference with mitotic spindle dynamics, inducing spindle collapse and, consequently, prolonged mitotic arrest, culminating in massive cancer cell death by apoptosis.

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Apoptosis Detection Methods in Diagnosis of Cancer and Their Potential Role in Treatment: Advantages and Disadvantages: a Review

Cited by 16 publications

References 71 publications

Licochalcone A induces cell cycle arrest and apoptosis via suppressing MAPK signaling pathway and the expression of FBXO5 in lung squamous cell cancer

Licochalcone A induces cell cycle arrest and apoptosis via suppressing MAPK signaling pathway and the expression of FBXO5 in lung squamous cell cancer

Chronic exposure to yttrium induced cell apoptosis in the testis by mediating Ca2+/IP3R1/CaMKII signaling

BP-M345 as a Basis for the Discovery of New Diarylpentanoids with Promising Antimitotic Activity

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