Molecular and Cellular Oncology最新文献

An antibody-drug conjugate for endometrioid carcinoma based on the expression of cell adhesion molecule 1. 基于细胞粘附分子 1 表达的子宫内膜样癌抗体-药物共轭物。

IF 2.6

Molecular and Cellular Oncology Pub Date : 2024-09-05 eCollection Date: 2024-01-01 DOI: 10.1080/23723556.2024.2399379

Man Hagiyama, Azusa Yoneshige, Tomoyuki Otani, Akihiro Wada, Fuka Takeuchi, Yuji Shoya, Takao Inoue, Akihiko Ito

{"title":"An antibody-drug conjugate for endometrioid carcinoma based on the expression of cell adhesion molecule 1.","authors":"Man Hagiyama, Azusa Yoneshige, Tomoyuki Otani, Akihiro Wada, Fuka Takeuchi, Yuji Shoya, Takao Inoue, Akihiko Ito","doi":"10.1080/23723556.2024.2399379","DOIUrl":"https://doi.org/10.1080/23723556.2024.2399379","url":null,"abstract":"Cell adhesion molecule 1 (CADM1), an immunoglobulin superfamily member, is expressed in endometrial glandular cells highly during the proliferative phase but lowly during the secretory phase. Previously, a CADM1-targeting antibody-drug conjugate (ADC) was generated, in which a humanized anti-CADM1 ectodomain antibody h3E1 was linked with monomethyl auristatin E (h3E1-MMAE ADC). The present study aimed at probing whether this ADC could be useful for the treatment of endometrial neoplasm. Firstly, immunohistochemistry for CADM1 was conducted on proliferative-phase endometrium (n = 13), endometrial hyperplasia (n = 35), and endometrioid carcinoma at various stages (n = 166). CADM1 immunostaining intensity was highest in atypical endometrial hyperplasia and endometrioid carcinoma confined within the endometrium and was decreased stepwise as the carcinoma stage progressed. Next, h3E1-MMAE ADC was examined for its cytotoxicity in vitro using human endometrial adenocarcinoma cell lines expressing CADM1; HEC-1B, HEC-50B, JHUM-3, and OMC-2. The ADC killed these cells in a dose-dependent manner with half maximal inhibitory concentration (IC50) of 12.02 nM for HEC-1B and 2.04 nM for HEC-50B. Collectively, h3E1-MMAE ADC may serve as a noninvasive alternative to simple hysterectomy in the treatment of endometrioid carcinoma confined within the endometrium.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11382700/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142297421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The SIRT7-nucleolus connection in cancer: ARF enters the fray. 癌症中 SIRT7 与核仁的联系：ARF 加入战局

IF 2.6

Molecular and Cellular Oncology Pub Date : 2024-07-17 eCollection Date: 2024-01-01 DOI: 10.1080/23723556.2024.2381287

Shahriar Tarighi, Poonam Kumari, Alejandro Vaquero, Thomas Braun, Alessandro Ianni

引用次数: 0

Amino acid deprivation in cancer cells with compensatory autophagy induction increases sensitivity to autophagy inhibitors. 癌细胞中氨基酸匮乏与自噬代偿诱导可增加对自噬抑制剂的敏感性。

IF 2.6

Molecular and Cellular Oncology Pub Date : 2024-07-14 eCollection Date: 2024-01-01 DOI: 10.1080/23723556.2024.2377404

Takahito Fukui, Manami Yabumoto, Misuzu Nishida, Shiori Hirokawa, Riho Sato, Taichi Kurisu, Miyu Nakai, Md Abul Hassan, Koji Kishimoto

{"title":"Amino acid deprivation in cancer cells with compensatory autophagy induction increases sensitivity to autophagy inhibitors.","authors":"Takahito Fukui, Manami Yabumoto, Misuzu Nishida, Shiori Hirokawa, Riho Sato, Taichi Kurisu, Miyu Nakai, Md Abul Hassan, Koji Kishimoto","doi":"10.1080/23723556.2024.2377404","DOIUrl":"10.1080/23723556.2024.2377404","url":null,"abstract":"Inhibition of autophagy is an important strategy in cancer therapy. However, prolonged inhibition of certain autophagies in established cancer cells may increase therapeutic resistance, though the underlying mechanisms of its induction and enhancement remain unclear. This study sought to elucidate the mechanisms of therapeutic resistance through repeated autophagy inhibition and amino acid deprivation (AD) in an in vitro model of in vivo chronic nutrient deprivation associated with cancer cell treatment. In the human cervical cancer cell line HeLa and human breast cancer cell line MCF-7, initial extracellular AD induced the immediate expression of endosomal microautophagy (eMI). However, repeated inhibition of eMI with U18666A and extracellular AD induced macroautophagy (MA) to compensate for reduced eMI, simultaneously decreasing cytotoxicity. Here, hyperphosphorylated JNK was transformed into a hypophosphorylated state, suggesting conversion of the cell death signal to a survival signal. In a nutrient medium, cell death could not be induced by MA inhibition. However, since LAT1 inhibitors induce intracellular AD, combining them with MA and eMI inhibitors successfully promoted cell death in resistant cells. Our study identified a novel therapeuic approach for promoting cell death and addressing therapeutic resistance in cancers under autophagy-inhibitor treatment.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11253891/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141634856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Selection forces underlying aneuploidy patterns in cancer. 癌症非整倍体模式背后的选择力量。

IF 2.6

Molecular and Cellular Oncology Pub Date : 2024-06-24 eCollection Date: 2024-01-01 DOI: 10.1080/23723556.2024.2369388

Tamara C Klockner, Christopher S Campbell

{"title":"Selection forces underlying aneuploidy patterns in cancer.","authors":"Tamara C Klockner, Christopher S Campbell","doi":"10.1080/23723556.2024.2369388","DOIUrl":"10.1080/23723556.2024.2369388","url":null,"abstract":"Aneuploidy, the presence of an aberrant number of chromosomes, has been associated with tumorigenesis for over a century. More recently, advances in karyotyping techniques have revealed its high prevalence in cancer: About 90% of solid tumors and 50-70% of hematopoietic cancers exhibit chromosome gains or losses. When analyzed at the level of specific chromosomes, there are strong patterns that are observed in cancer karyotypes both pan-cancer and for specific cancer types. These specific aneuploidy patterns correlate strongly with outcomes for tumor initiation, progression, metastasis formation, immune evasion and resistance to therapeutic treatment. Despite their prominence, understanding the basis underlying aneuploidy patterns in cancer has been challenging. Advances in genetic engineering and bioinformatic analyses now offer insights into the genetic determinants of aneuploidy pattern selection. Overall, there is substantial evidence that expression changes of particular genes can act as the positive selective forces for adaptation through aneuploidy. Recent findings suggest that multiple genes contribute to the selection of specific aneuploid chromosomes in cancer; however, further research is necessary to identify the most impactful driver genes. Determining the genetic basis and accompanying vulnerabilities of specific aneuploidy patterns is an essential step in selectively targeting these hallmarks of tumors.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2024-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11197905/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141451814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Clemastine and hyperthermia enhance sensitization of osteosarcoma cells for apoptosis. 氯马斯汀和热疗可增强骨肉瘤细胞对凋亡的敏感性。

IF 2.1

Molecular and Cellular Oncology Pub Date : 2024-05-14 eCollection Date: 2024-01-01 DOI: 10.1080/23723556.2024.2351622

Somtochukwu Obu, Suryakant Niture, Hieu Hoang, Sashi Gadi, Vandana, Yiping He, Deepak Kumar

{"title":"Clemastine and hyperthermia enhance sensitization of osteosarcoma cells for apoptosis.","authors":"Somtochukwu Obu, Suryakant Niture, Hieu Hoang, Sashi Gadi, Vandana, Yiping He, Deepak Kumar","doi":"10.1080/23723556.2024.2351622","DOIUrl":"10.1080/23723556.2024.2351622","url":null,"abstract":"Clemastine is an antagonist of histamine H1 receptor may provide benefits in the treatment of osteosarcoma (OS). In the current study, we used hyperthermia approach to sensitize OS cells to clemastine-mediated cell death. Osteosarcoma U-2 OS and Saos-2 cells were treated with clemastine at 37°C, followed by 42°C for 2 h, and released at 37°C for 6 h. The impact of clemastine and hyperthermia on OS cell survival and autophagy-mediated cell death was investigated. Exposure of U-2 OS and Saos-2 cells to clemastine and hyperthermia (42°C) inhibited dose-dependent clemastine-mediated cell survival by increasing cell apoptosis. Hyperthermia and clemastine exposure modulated inflammatory and unfolded protein response (UPR) signaling differentially in U-2 OS and Saos-2 cells. Exposure of U-2 OS and Saos-2 cells to hyperthermia and clemastine inhibited AKT/mTOR and induced expression of the autophagy biomarkers LC3B II and LC3-positive puncta formation. The inhibition of autophagy by 3-methyladenine blocked hyperthermia and clemastine-mediated induction of LC3B II, LC3-positive puncta formation, and OS cell apoptosis. These results indicate that clemastine and hyperthermia sensitize OS cell lines by inducing increased autophagic cell death. Collectively, our data suggest that hyperthermia along with antihistamine therapy may provide an improved approach for the treatment of OS.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11110698/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141082620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Regulation of Med1 protein by overexpression of BAP1 in breast cancer cells. 乳腺癌细胞中 BAP1 的过表达对 Med1 蛋白的调控

IF 2.1

Molecular and Cellular Oncology Pub Date : 2024-05-02 eCollection Date: 2024-01-01 DOI: 10.1080/23723556.2024.2347827

Hyunju Kim

{"title":"Regulation of Med1 protein by overexpression of BAP1 in breast cancer cells.","authors":"Hyunju Kim","doi":"10.1080/23723556.2024.2347827","DOIUrl":"https://doi.org/10.1080/23723556.2024.2347827","url":null,"abstract":"Med1 binds to a nuclear receptor and regulates transcription. Elevated Med1 protein expression promotes cancer growth in hormone-dependent breast and prostate cancers. Med1 protein expression was investigated by deubiquitinating enzymes (DUBs) overexpression in breast cancer cell lines. Various DNA constructs of SRT-DUBs were overexpressed in the MCF7 cell line, and Med1 protein expression was investigated by western blotting. The cell growth and in vitro invasion assay were performed in BRCA1-associated protein 1 (BAP1) wild type and mutant (C91A) overexpressed cells. Ubiquitination of the Med1 protein was observed, and Med1 protein expression and transcriptional activity were verified by various DUBs overexpressed. Although Med1 protein expression increased upon the overexpression of BAP1, it was not affected by the overexpression of BAP1 mutant (C91A). BAP1 was increased by the E2 treatment, which has an important effect on the breast cancer growth, and cell growth was decreased by BAP1 C91A overexpression. However, metastatic capacities were decreased by BAP1. In addition, the binding between the Med1 and the BAP1 protein was observed. These data suggested that BAP1 regulated Med1 protein expression in breast cancer cells and involved in cancer cell growth and metastasis by binding to Med1 protein.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11067983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140855430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Molecular analysis to identify novel potential biomarkers as drug targets in colorectal cancer therapy: an integrated bioinformatics analysis. 通过分子分析确定结直肠癌治疗中作为药物靶点的新型潜在生物标记物：综合生物信息学分析。

IF 2.1

Molecular and Cellular Oncology Pub Date : 2024-03-18 eCollection Date: 2024-01-01 DOI: 10.1080/23723556.2024.2326699

Mansour K Gatasheh, Sathan Raj Natarajan, Rajapandiyan Krishnamoorthy, Tawfiq S Alsulami, Ponnulakshmi Rajagopal, Chella Perumal Palanisamy, Vishnu Priya Veeraraghavan, Selvaraj Jayaraman

{"title":"Molecular analysis to identify novel potential biomarkers as drug targets in colorectal cancer therapy: an integrated bioinformatics analysis.","authors":"Mansour K Gatasheh, Sathan Raj Natarajan, Rajapandiyan Krishnamoorthy, Tawfiq S Alsulami, Ponnulakshmi Rajagopal, Chella Perumal Palanisamy, Vishnu Priya Veeraraghavan, Selvaraj Jayaraman","doi":"10.1080/23723556.2024.2326699","DOIUrl":"https://doi.org/10.1080/23723556.2024.2326699","url":null,"abstract":"Colorectal cancer (CRC) is a heterogeneous disease that requires new diagnostic and prognostic markers. Integrated bioinformatics approach to identify novel therapeutic targets associated with CRC. Using GEO2R identified DEGs in CRC, and Funrich software facilitated the visualization of DEGs through Venn diagrams. From a total of 114 enhanced DEGs, potential hub genes were further filtered based on their nodal strength and edges using STRING database. To gain insights into the functional roles of these hub genes, gene ontology and pathway enrichment were conducted thorough g: profiler web server. Subsequently, overall survival plots from GEPIA and oncogenic predictive functions like mRNA expressions for stages and nodal metastasis were employed to identify hub genes in CRC patient samples. Additionally, the cBioPortal and HPA databases also revealed genetic alterations and expression levels in these hub genes in CRC patients, further supporting their involvement in colorectal cancer. Gene expression by RT-PCR shows upregulation of hub genes in HT-29 cells. Finally, our integrated bioinformatic analysis revealed that ABCE1, AURKA, HSPD1, PHKA1, CDK4, and YWHAE as hub genes with potential oncogenic roles in CRC. These genes hold promise as diagnostic and prognostic markers for colorectal tumorigenesis, providing insights into targeted therapies for improved patient outcomes.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10950290/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140176901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mass spectrometry-based proteomic analysis to characterize cisplatin induced early signaling events in head and neck squamous cell carcinoma. 基于质谱的蛋白质组分析，描述头颈部鳞状细胞癌中顺铂诱导的早期信号事件。

IF 2.1

Molecular and Cellular Oncology Pub Date : 2024-03-13 eCollection Date: 2024-01-01 DOI: 10.1080/23723556.2024.2328873

Ankit P Jain, Vivek Ghose, Srijon Munshi, Firdous A Bhat, Gourav Dey, Vishalakshi Nanjappa

{"title":"Mass spectrometry-based proteomic analysis to characterize cisplatin induced early signaling events in head and neck squamous cell carcinoma.","authors":"Ankit P Jain, Vivek Ghose, Srijon Munshi, Firdous A Bhat, Gourav Dey, Vishalakshi Nanjappa","doi":"10.1080/23723556.2024.2328873","DOIUrl":"10.1080/23723556.2024.2328873","url":null,"abstract":"Cisplatin is the commonly used chemotherapeutic drug in treatment of various cancers. However, development of resistance towards cisplatin results in tumor recurrence. Here, we aim to understand the mechanisms of action of cisplatin and emergence of resistance to cisplatin using mass spectrometry-based proteomic approach. A panel of head and neck squamous cell carcinoma (HNSCC) cell lines were treated with cisplatin at respective IC50 for 24 h and label-free mass spectrometry analysis was carried out. Proteomic analysis of A253, FaDu, Det562 and CAL27 cell lines upon cisplatin treatment resulted in the identification of 5,060, 4,816, 4,537 and 4,142 proteins, respectively. Bioinformatics analysis of differentially regulated proteins revealed proteins implicated in DNA damage bypass pathway, translation and mRNA splicing to be enriched. Further, proteins associated with cisplatin resistance exhibited alterations following short-term cisplatin exposure. Among these, class III tubullin protein (TUBB3) was found to be upregulated in cisplatin-treated cells compared to untreated cells. Western blot analysis confirmed the elevated expression of TUBB3 in cells treated with cisplatin for 24 h, and also in cisplatin resistant HNSCC cell lines. This study delineates the early signaling events that enable HNSCC cells to counteract the cytotoxic effects of cisplatin and facilitate the development of resistance.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10939151/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140132805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Hypofunction of macrophage chemotaxis contributes to defective efficacy of herceptin in HER2-positive breast cancer patients. 巨噬细胞趋化功能低下导致赫赛汀对HER2阳性乳腺癌患者的疗效缺陷

IF 2.1

Molecular and Cellular Oncology Pub Date : 2024-02-07 eCollection Date: 2024-01-01 DOI: 10.1080/23723556.2024.2309715

Yu Song, Qiao-Chen Geng, Wen-Jing An, Fu-Cheng Zhang, Ran Jiang, Rui-Sheng Zhao, Zhi-Jian Deng, Heng Li

{"title":"Hypofunction of macrophage chemotaxis contributes to defective efficacy of herceptin in HER2-positive breast cancer patients.","authors":"Yu Song, Qiao-Chen Geng, Wen-Jing An, Fu-Cheng Zhang, Ran Jiang, Rui-Sheng Zhao, Zhi-Jian Deng, Heng Li","doi":"10.1080/23723556.2024.2309715","DOIUrl":"https://doi.org/10.1080/23723556.2024.2309715","url":null,"abstract":"Breast cancer was considered as a kind of prone breast tumors with the complicated pathological mechanisms and diverse clinical classifications. In the clinical treatments of HER2-positive tumor patients, HER2 monoclonal antibodies, such as Herceptin, have shown well-defined therapeutic effects. Nevertheless, due to the heterogeneity of breast cancers, drug resistance inevitably appeared during the application of Herceptin. In order to fully understand the immune tolerance status of the tumor microenvironment in the population of sensitive and insensitive patients, this study carried out a series of studies through Luminex cytokines assay, clinicopathological analysis, immunofluorescence, and PCR. The results confirmed that in clinical samples sensitive to Herceptin, there were a large number of macrophages, and the protein expression levels and in situ expression of macrophage-related chemokines and inflammatory mediators are significantly higher than drug-resistant tumor samples. Further studies found that T cell function has a low correlation with tumor growth, and there are obvious obstacles in the process of peripheral blood immune cells entering the tumor microenvironment. In summary, this study provided clues for understanding the clinical drug resistance of HER2 monoclonal antibody and the clinical rational use of drugs and combination drugs.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10854276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139724322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mangifera indica L. kernel ethanol extract inhibits cell viability and proliferation with induction of cell cycle arrest and apoptosis in lung cancer cells. 芒果核乙醇提取物可抑制肺癌细胞的活力和增殖，并诱导细胞周期停滞和凋亡。

IF 2.1

Molecular and Cellular Oncology Pub Date : 2024-01-04 eCollection Date: 2024-01-01 DOI: 10.1080/23723556.2023.2299046

Hussah Abdullah Alshwyeh, Warqaa Muhammed Shariff Al-Sheikh, Abdullah Rasedee, Sulaiman Mohammed Alnasser, Mothanna Sadiq Al-Qubaisi, Wisam Nabeel Ibrahim

{"title":"Mangifera indica L. kernel ethanol extract inhibits cell viability and proliferation with induction of cell cycle arrest and apoptosis in lung cancer cells.","authors":"Hussah Abdullah Alshwyeh, Warqaa Muhammed Shariff Al-Sheikh, Abdullah Rasedee, Sulaiman Mohammed Alnasser, Mothanna Sadiq Al-Qubaisi, Wisam Nabeel Ibrahim","doi":"10.1080/23723556.2023.2299046","DOIUrl":"10.1080/23723556.2023.2299046","url":null,"abstract":"In this study, we investigated the effects of an ethanolic extract of Mangifera indica L. kernel on the viability and proliferation of human lung cancer cells. We utilized MTT and BrdU cell proliferation assays, morphological assessments, cell cycle analyses, and apoptosis assays to investigate the extract's effects on lung cancer (A549 and NCI-H292) and normal lung (MRC-5) cells. The extract demonstrated a toxicity toward cancer cells compared to normal cells with dose-dependent anti-proliferative effect on lung cancer cells. The extract also caused differential effects on the cell cycle, inducing G0/G1 arrest and increasing the Sub-G1 population in both lung cancer and normal lung cells. Notably, the extract induced loss of membrane integrity, shrinkage, membrane blebbing, and apoptosis in lung cancer cells, while normal cells exhibited only early apoptosis. Furthermore, the extract exhibited higher toxicity towards NCI-H292 cells, followed by A549 and normal MRC-5 cells in decreasing order of potency. Our results suggest that the ethanolic extract of M. indica L. kernel has significant potential as a novel therapeutic agent for treating lung cancer cells, given its ability to induce apoptosis in cancer cell lines while causing minimal harm to normal cells.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10773660/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139404723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0