scholarly journals Psiadin and plectranthone selectively inhibit colorectal carcinoma cells proliferation via modulating cyclins signaling and apoptotic pathways

PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0252820
Author(s):  
Khaled Y. Orabi ◽  
Mohamed S. Abaza ◽  
Yunus A. Luqmani ◽  
Rajaa Al-Attiyah
Keyword(s):  
Colorectal Carcinoma ◽  
Cancer Cells ◽  
Cell Lines ◽  
Molecular Mechanisms ◽  
Therapeutic Potential ◽  
Normal Breast ◽  
Dependent Manner ◽  
Isolation And Purification ◽  
Apoptotic Pathways ◽  
Dose Dependent

Three scarce terpenes, psiadin, plectranthone and saudinolide, were obtained after chromatographic isolation and purification from the aerial parts of the respective plants. Their identities were established based on their spectral data. Their anticancer effects against two human colorectal carcinoma cell lines, CCL233 and CCL235, along with the potential molecular mechanisms of action, were explored. Psiadin and plectranthone exhibited marked growth inhibition on both cell lines in a time- and dose-dependent manner with minimal cytotoxicity against normal breast cells (HB2). The terpenes even showed superior activities to the tested standards. Flow cytometry showed apoptosis induction and alteration in the cell cycle in colorectal cancer cells treated with both compounds. Nevertheless, it was also found that both compounds inhibited NF-κB transcriptional activity, induced mitochondrial membrane potential depolarization and increased the percentage of reactive oxygen species in the treated cancer cells in a dose-dependent manner as well. Since the anticancer effect of psiadin on cancer cells was higher than that produced by plectranthone, only psiadin was tested to determine its possible targets. The results suggested a high degree of specificity of action affecting particular cellular processes in both cancer cells. In conclusion, both terpenes, in particular psiadin, showed significant discriminative therapeutic potential between cancer and normal cells, a value that is missing in current chemotherapies.

Momordica charantia Seed and Aryl Extracts Potentiate Growth Inhibition and Apoptosis by Dual Blocking of PI3K/AKT and MAPK Pathways as a Downstream Target of EGFR Signaling in Breast Cancer Cells

2020 ◽  
Vol 16 (5) ◽  
pp. 726-733
Author(s):  
Guzide Satir Basaran ◽  
Hatice Bekci ◽  
Ayse Baldemir ◽  
Selen Ilgun ◽  
Ahmet Cumaoglu
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Breast Cancer Cells ◽  
Molecular Mechanisms ◽  
Therapeutic Potential ◽  
Momordica Charantia ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Seed Extracts

Background and Objective: Herbal extracts and plant compounds are increasingly becoming of interest for their therapeutic potential in various cancer types. Momordica charantia is well known for its anti-diabetic, anti-inflammatory, and anti-cancer properties. Methods: In the present study, we investigated the antiproliferative and pro-apoptotic effects of Momordica charantia seed and aryl extracts on breast cancer cells and explored the underlying molecular mechanisms. Results: Our results showed that both extract significantly inhibited the growth of MCF-7 and MDA MB-231 cells in a concentration-dependent manner, and induced apoptosis by upregulation of caspase 9 and caspase 3 mRNA levels. In addition, in different incubation time, both extract evidently inhibited EGF and induced EGFR phosphorylation/activation in both cell lines. Moreover, Momordica charantia aryl and seed extracts inhibited phosphorylation/activation of PI3K/AKT and MAPK (ERK and P38) pathways in both cell lines. Conclusion: The current study clearly demonstrates that the Momordica charantia aryl and seed extracts have the potential to exert its cytotoxic effect on breast cancer cells by a mechanism involving inhibition of EGFR and EGRF related pathways with the induction of apoptosis. The overall finding demonstrates that this plant, especially seed extract, could be a potential source of new anticancer compounds for possible drug development against cancer.

scholarly journals Nuclear upregulation of PI3K p110β correlates with increased rRNA transcription in endometrial cancer cells

2019 ◽  
Author(s):  
Fatemeh Mazloumi Gavgani ◽  
Thomas Karlsson ◽  
Ingvild L Tangen ◽  
Andrea Papdiné Morovicz ◽  
Victoria Smith Arnesen ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Molecular Mechanisms ◽  
Pi3k Pathway ◽  
Clinical Samples ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Cytoplasmic Staining ◽  
Ec Cells

AbstractGenes encoding for components of the phosphoinositide 3-kinase (PI3K) pathway are frequently mutated in cancer, including inactivating mutations of PTEN and activating mutations of PIK3CA, encoding the PI3K catalytic subunit p110α. PIK3CB, encoding p110β, is rarely mutated, but can contribute to tumourigenesis in some PTEN-deficient tumours. The underlying molecular mechanisms are however poorly understood. By analysing cell lines and annotated clinical samples, we have previously found that p110β is highly expressed in endometrial cancer (EC) cell lines and that PIK3CB mRNA levels increase early in primary tumours correlating with lower survival. Selective inhibition of p110α and p110β led to different effects on cell signalling and cell function, p110α activity being correlated to cell survival in PIK3CA mutant cells and p110β with cell proliferation in PTEN-deficient cells. To understand the mechanisms governing the differential roles of these isoforms, we assessed their sub-cellular localisation. p110α was cytoplasmic whereas p110β was both cytoplasmic and nuclear with increased levels in both compartments in cancer cells. Immunohistochemistry of p110β in clinically annotated patient tumour sections revealed high nuclear/cytoplasmic staining ratio, which correlated significantly with higher grades. Consistently, the presence of high levels of p110β in the nuclei of EC cells, correlated with high levels of its product phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P3) in the nucleus. Using immunofluorescence labelling, we observed both p110β and PtdIns(3,4,5)P3 in the nucleoli of EC cell lines. The production of nucleolar PtdIns(3,4,5)P3 was dependent upon p110β activity. EC cells with high levels of nuclear PtdIns(3,4,5)P3 and p110β showed elevated nucleolar activity as assessed by the increase in 47S pre-rRNA transcriptional levels in a p110β-dependent manner. Altogether, these results present a nucleolar role for the PI3K pathway that may contribute to tumour progression in endometrial cancer.

scholarly journals Anticancer Potential of Fruit Extracts from Vatica diospyroides Symington Type SS and Their Effect on Program Cell Death of Cervical Cancer Cell Lines

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Atchara Chothiphirat ◽  
Kesara Nittayaboon ◽  
Kanyanatt Kanokwiroon ◽  
Theera Srisawat ◽  
Raphatphorn Navakanitworakul
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Morphological Changes ◽  
Annexin V ◽  
Siha Cell ◽  
Caspase 8 ◽  
Dependent Manner ◽  
Cervical Cancer Cells ◽  
Dose Dependent

Vatica diospyroides Symington is locally known as Chan-Ka-Pho in Thailand. Ancient people have used it as therapeutic plant for cardiac and blood tonic cure. The purpose of this study was to investigate the potential cytotoxicity and selectivity of the extracts from V. diospyroides type SS fruit on cervical cancer HeLa and SiHa cell lines and to examine its underlying mechanism of action. MTT assay revealed that the extracts showed inhibition of cell survival in a dose-dependent manner and exhibited highly cytotoxic activity against both HeLa and SiHa cells with IC50 value less than 20 μg/mL along with less toxicity against L929 cells. Acetone cotyledon extract (ACE) showed the best selectivity index value of 4.47 (HeLa) and 3.51 (SiHa). Distinctive morphological changes were observed in ACE-treated cervical cancer cells contributing to apoptosis action. Flow cytometry analysis with Annexin V-FITC and PI staining precisely indicated that ACE induced apoptosis in HeLa and SiHa cell lines in a dose-dependent manner. Treatment of ACE with half IC50 caused DNA fragmentation and also activated increasing of bax and cleaved caspase-8 protein in HeLa cells after 48 h exposure. The results suggest that ACE has potent and selective cytotoxic effect against cervical cancer cells and the potential to induce bax and caspase-8-dependent apoptosis. Hence, the ACE could be further exploited as a potential lead in cancer treatment.

The EGFR-Inhibitor Erlotinib Induces Apoptosis in Neoplastic Cells of Myelodysplastic Syndrome (MDS) and Acute Myeloid Leukemia (AML), an Effect Determined by the Expression Level of Nucleophosmin (NPM).

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 856-856
Author(s):  
Simone Boehrer ◽  
Lionel Ades ◽  
Claire Fabre ◽  
Pierre Fenaux ◽  
Guido Kroemer
Keyword(s):  
Cell Lines ◽  
Molecular Mechanisms ◽  
Therapeutic Potential ◽  
Ex Vivo ◽  
Myeloid Cell ◽  
Expression Level ◽  
Apoptotic Cells ◽  
Dependent Manner ◽  
Egfr Inhibitor ◽  
Down Regulation

Abstract Background: the epidermal-growth-factor-receptor (EGFR)-inhibitor erlotinib was rationally designed to antagonize the deregulated EGFR-activity in solid tumors. Abundant studies in these entities not only demonstrated clinical efficacy, but also a favorable toxicity profile. In particular the absence of hematopoietic toxicity prompted us to investigate the therapeutic potential of erlotinib in MDS and AML cells. Methods: We incubated ex vivo cells from patients with MDS (n=4, 2 lower risk and 2 higher risk) and AML (n=6, de novo: 3; post MDS: 3), as well as a broad spectrum of myeloid cell lines (P39, KG-1, HL-60, MV4-11, MOLM-13) with increasing dosages of erlotinib (1μM to 10μM). As controls (n=4) we used non-malignant CD34 + bone marrow cells. Before incubation, all ex vivo cells underwent CD34 + selection. Serial FACS-analyses of parameters determining apoptosis (DIOC/PI and AnnexinV/PI) were carried out over a maximum of 6 days. Results: We found that erlotinib was able to induce a considerable degree of apoptosis in MDS and AML cells. Although there was a high interindividual difference in sensitivity towards erlotinib, “responders” treated with 10μM erlotinib showed an increase of apoptotic cells between 20–30% after 72h, which reached a maximum of 60% on day 6. This apoptosis-inducing effect was achieved in a dose-dependent manner and not restricted to a specific entity. Noteworthy, erlotinib exhibited no toxicity towards non-neoplastic progenitor cells. Evaluating the molecular mechanisms determining sensitivity we showed that the apoptosis-inducing effect of erlotinib critically depended on the expression level of NPM. Thus erlotinib-resistant myeloid cell lines (i.e. P39) exhibited a higher epression of NPM than sensitive cell lines (i.e. KG-1). In addition, down-regulation of NPM by small-interfering RNA not only increased the apoptosis-inducing effect of erlotinib in sensitive cells, but moreover established sensitivity in otherwise erlotinib-resistant cells. Accordingly, siRNA-induced down-regulation of NPM in P39 cells elevated the percentage of apoptotic cells upon treatment with 10μM erlotinib by about 30% as compared to mock-transfected controls. Conclusion, we showed an off-target effect of erlotinib, as evidenced by its ability to induce apoptosis in EGFR-negative cells. Of particular interest is the observation that erlotinib induced apoptosis exclusively in neoplastic myeloid cells while sparing non-malignant progenitors. To the best of our knowledge, this is the first report providing evidence for the therapeutic potential of erlotinib in MDS and AML.

scholarly journals Evaluation of Terpenes Psiadin, Plectranthone, and Saudinolide as Selective Anti-Cancer Agents against Hepatic Carcinoma Cells

2020 ◽  
Author(s):  
Khaled Y. Orabi ◽  
Mohamed S. Abaza ◽  
Rajaa Al-Attiyah ◽  
Yunus A. Luqmani
Keyword(s):  
Cell Cycle ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cell Cycle Progression ◽  
Molecular Mechanisms ◽  
Therapeutic Potential ◽  
Cancer Cell Lines ◽  
Chemotherapeutic Agents ◽  
Isolation And Purification

: Plant-derived terpenes have aroused considerable interest as chemotherapeutic agents for a variety of diseases. This study aimed at the isolation and purification of the scarce terpenes psiadin, plectranthone and saudinolide from their respective plants, followed by the determination of antiproliferative activity, against hepatic cancer cell lines (HepG2, Hep3B), and the potential molecular mechanisms. Time- and dose-dependent cytotoxicity, evaluated using MTT and colony-forming assays, were exhibited by psiadin and plectranthone against the cancer cells. Flow cytometry showed that these two terpenes blocked cell cycle progression and induced mitochondrial-mediated apoptosis, particularly through increased cytochrome c and disruption of mitochondrial membrane potential. Additionally, they initiated the generation of reactive oxygen species as well as inhibiting NF-B. Psiadin lowered several essential cyclins and cyclin-dependent kinases and reduced RB activation. It was concluded that psiadin, in particular, has a significant therapeutic potential with the biggest advantage of differentiating between cancer and normal cells which is acutely lacking in current cytotoxic drugs. Its precise mode of action needs further investigation but appears predominantly to cause cell cycle arrest by interfering with cyclin production. It will be important to determine, in future studies, whether these terpenes will similarly inhibit other cancer cell lines and retain its activity against tumors in vivo.

Regulation of Histone Deacetylase in Waldenström Macroglobulinemia

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 2617-2617
Author(s):  
Xiaoying Jia ◽  
Aldo M. Roccaro ◽  
Abdel Kareem Azab ◽  
Hai T. Ngo ◽  
Antonio Sacco ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Western Blot ◽  
Histone Deacetylase ◽  
Cell Lines ◽  
Parp Cleavage ◽  
Low Grade ◽  
Dependent Manner ◽  
Apoptotic Pathways ◽  
Dose Dependent

Abstract Background: Waldenström’s Macroglobulinemia (WM) is an incurable lymphoplasmacytic lymphoma with limited options of therapy. Histone deacetylase (HDAC) inhibitors represent promising new treatment strategy in B cell malignancies. We therefore investigated the in vitro effect of the novel hydroxamic acid derivative HDAC inhibitor LBH589 in WM. Methods: WM cell lines (BCWM1 and WSU-WM) and IgM secreting low-grade lymphoma cell lines (MEC1, RL) were used. Bone marrow primary CD19+ cells and bone marrow stromal cells (BMSC) were obtained from patients with WM after informed consent. Cytotoxicity and DNA synthesis were measured by MTS assay and thymidine uptake assay. Cell signaling and apoptotic pathways were determined by Western Blot and immunofluorescence. Results: LBH589 induced a significant decrease of proliferation and triggered cytotoxicity in all cell lines tested and primary CD19+ WM cells (IC50 of 20–40nM), even in the presence of BMSC, IL-6 and IGF-1, which induce resistance to conventional therapies. Importantly, LBH589 did not induce cytotoxicity in healthy donor peripheral blood mononuclear cells. LBH589 induced both intrinsic and extrinsic apoptotic pathways, with caspase-9, caspase-8, caspase-3, and PARP cleavage in a dose-dependent manner. We also demonstrated significant upregulation of the proapoptotic transcription factor p53 and down-regulation of the anti-apoptotic proteins BclxL, Mcl-1 and c-myc. We then demonstrated that LBH589 induced apoptosis in WM cells in a caspase-independent manner through induction of autophagy, as shown by upregulation of LC3B and Rab7 expression. We further determined the mechanism of action of LBH589 in WM, investigating the effect of LBH589 on histone acetylation and NF-kB pathways. We found that LBH589 induced a dose-dependent increase in histone H3-H4 acetylation; and inhibited both canonical and non-canonical pathways of NF-κB, as shown by western blot and immunofluorescence. In addition, LBH589 augmented rituximab, fludarabine, bortezomib, and perifosine-induced cyotoxicity in WM cells. Conclusion: LBH589 has significant antitumor activity in WM in vitro, providing the framework for clinical trials evaluating LBH589 as a new therapeutic agent in patients with WM.

scholarly journals Abyssinone V-4′ Methyl Ether, a Flavanone Isolated from Erythrina droogmansiana, Exhibits Cytotoxic Effects on Human Breast Cancer Cells by Induction of Apoptosis and Suppression of Invasion

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Stéphane Zingue ◽  
Abel Joël Gbaweng Yaya ◽  
Julia Cisilotto ◽  
Larissa Vanelle Kenmogne ◽  
Emmanuel Talla ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Cell Lines ◽  
Methyl Ether ◽  
Breast Cancer Cells ◽  
Molecular Mechanisms ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Cytotoxic Effects

Abyssinone V-4′ methyl ether (AVME) isolated from Erythrina droogmansiana was recently reported to exhibit anti-mammary tumor effect in mice. The present work was therefore aimed at elucidating its cellular and molecular mechanisms. To achieve our goal, the cytotoxicity of AVME against tumoral and non-tumoral cell lines was evaluated by resazurin reduction test; flow cytometry allowed us to evaluate the cell cycle and mechanisms of cell death; the mitochondrial transmembrane potential, reactive oxygen species (ROS) levels, and caspase activities as well as apoptosis-regulatory proteins (Bcl-2 and Bcl-XL) were measured in MDA-MB-231 cells. Further, the antimetastatic potential of AVME was evaluated by invasion assay. AVME exhibited cytotoxic effects in all tested tumor cell lines and induced a significant increase in the percentage of MDA-MB-231 cells at G2/M and S phases of the cell cycle in a concentration-dependent manner. AVME also induced apoptosis in MDA-MB-231 cells, which was accompanied by the activation of caspase-3 and caspase-9 and downregulation of Bcl-2 and Bcl-XL proteins. Moreover, AVME suppressed cancer cell invasion by the inhibition of the metalloproteinase-9 activity. Findings from this study suggest that AVME has anti-breast cancer activities expressed through mitochondrial proapoptotic pathway including impairment of aggressive behaviors of breast cancer cells.

scholarly journals Cytotoxic Effect on Cancer Cells and Structural Identification of Phenols from Spatholobi Caulis by HPLC-ESI-MSn

2009 ◽  
Vol 4 (6) ◽  
pp. 1934578X0900400 ◽  
Author(s):  
Dan Lu ◽  
Hua He ◽  
Bin Wu ◽  
Shanjing Yao
Keyword(s):  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cytotoxic Effect ◽  
Human Cancer ◽  
Cancer Cell Lines ◽  
Screening Tests ◽  
Hl60 Cell ◽  
Dependent Manner ◽  
Dose Dependent

To find fractions from Spatholobi caulis with cytotoxic effects on cancer cell lines, screening tests were carried out using the SRB assay on the HL60 cell line. Further investigation with HL60 and another four human cancer cell lines (KB, K562, MCF-7 and Hep G2), revealed a dose-dependent response. High-performance liquid chromatography coupled with electrospray ionization-tandem mass spectrometry (HPLC- ESI-MSn) was used to isolate and identify the active constituents from the active fraction. Three fractions (F-IV, F-V and F-VII) showed in vitro cytotoxicity. F-V inhibited the growth of cancer cells in a dose-dependent manner. The IC50 values for KB, K562 and HL60 cells were 17.6, 8.3 and 9.7 μg/mL, respectively. The dominating constituents of F-V were either identified or tentatively characterized as nine phenolic compounds, eight isoflavones and 9-methoxycoumestrol. The isoflavones 7-hydroxy-3′,4′-dimethoxy isoflavone, 7-hydroxy-6,2′,4′-trimethoxy isoflavone and 3′-hydroxy-7,4′-dimethoxy isoflavone are reported for the first time for Spatholobi caulis. The results suggest that these compounds contribute to the cytotoxic effect of Spatholobi caulis.

Halofuginone, an Old Anticoccidosis Drug, Induces Apoptosisin Multiple Myeloma Cells, Associated with Down Regulation of MCL1.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4786-4786
Author(s):  
Merav Leiba ◽  
Yu-Tzu Tai ◽  
Teru Hideshima ◽  
Jana Jakubikova ◽  
Ikeda Hiroshi ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Cell Lines ◽  
Molecular Mechanisms ◽  
Caspase 3 ◽  
Mononuclear Cells ◽  
Matrix Metalloproteinase 2 ◽  
Type I ◽  
Dependent Manner ◽  
Peripheral Blood Mononuclear ◽  
Dose Dependent

Abstract Halofuginone, a synthetic derivative of quinazolinone alkaloid, has recently been shown to have an anti-cancer effect in various solid and hematological malignancies. It is an orally available drug with a safe toxicity profile in clinical trials of inflammatory disease and has anti-angiogenic, anti-metastatic and anti-proliferative effects in preclinical studies. It blocks TGFb signaling by targeting Smad 2/3, inhibits NFkB activity, as well as downregulates extra cellular matrix (ECM) formation via the inhibition of collagen type I formation and matrix metalloproteinase 2(MMP2). Since ECM has an important role in the bone marrow microenvironment in multiple myeloma (MM) pathogenesis, we here examined whether halofuginone induces cytotoxicity against various MM cell lines, including those sensitive and resistant to conventional and novel chemotherapies. Halofuginone (12.5–400 nM) induced cytotoxicity in a dose-dependent fashion in a variety of MM cell lines (n=20), regardless of the sensitivity to conventional chemotherapy (i.e., dexamethasone, melphalan, doxorubicin) and novel therapies (i.e., lenalidomide, bortezomib) with IC50 of 50–200 nM. In contrast, halofuginone did not induce cytotoxicity against CD40-activated peripheral blood mononuclear cells from normal donors, even at high doses (500–1000nM). Importantly, neither IL6 nor IGF1, two key growth and survival factors in MM, overcame the growth inhibitory effect of halofuginone. We further examined molecular mechanisms whereby halofuginone triggers growth inhibition in MM cells. It induced both apoptosis and necrosis in a time- (2–48h) and dose (50–200 nM) dependent manner in MM1R and OPM1 MM cells, assessed by annexin V/ PI staining. Significant dose- dependent activation of caspase 3 and 8 was demonstrated after 25–200 nM of halofuginone treatment of MM1R, MM1S, and OPM1 cells. Mitochondrial membrane potential was also reduced after 24 hours of halofuginone treatment (50, 200 nM) of MM1R and OPMI cells, as evident by the accumulation of JC1 monomers. In addition, western blot analysis showed that halofuginone induces cleavage of apoptotic proteins caspase 3/8 and PARP, and downregulates anti-apoptotic protein MCL1. Taken together, these data suggest that halofuginone has significant anti-MM activities and is a potential novel therapy in MM.

scholarly journals Sanguinarine Mediated Anti-Tumor activity Via Targeting JAK/STAT3 Pathway in Thyroid Cancer

2020 ◽  
Author(s):  
Elham Ahmed ◽  
Abdul Khan ◽  
Kirti S. Prabhu ◽  
Kodappully Siveen ◽  
Zafar Nawaz ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cell Lines ◽  
Caspase 3 ◽  
Therapeutic Potential ◽  
Dependent Manner ◽  
Pharmacological Activities ◽  
Anti Cancer ◽  
Anti Tumor Activity ◽  
Dose Dependent ◽  
Inhibit Cell Proliferation

Sanguinarine (SNG), a natural compound with an array of pharmacological activities, has promising therapeutic potential against a number of pathological conditions, including malignancies. This research aimed to investigate the antiproliferative and anti-cancer potential of SNG against two well characterized papillary thyroid cancer (PTC) cell lines, BCPAP and TPC-1 .In both cell lines , SNG was able to inhibit cell proliferation in time and dose dependent manner. Western blot analysis revealed increased expression of apoptosis and autophagy markers , caspase-3,cleaved caspase-3 , P62, and LC3. SNG modulate its anticancer effect through ROS production, because NAC was able to reverse SNG effect. Interestingly, co-treatment of PTC with SNG and cisplatin amplified anticancer activity. Finally, SNG treatment of PTC spheroid suppressed its growth with downregulation of stemness markers including ALDH2 and SOX2 markers. In conclusion, SNG enhanced the anti cancer activity against PTC cells and the effect is amplified when cisplatin is added.

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