Category: 347174-05-4

Du, Xing; Zhang, Jingjing; Liu, Ling; Xu, Bo; Han, Hang; Dai, Wenjie; Pei, Xiuying; Fu, Xufeng; Hou, Shaozhang published the artcile< A novel anticancer property of Lycium barbarum polysaccharide in triggering ferroptosis of breast cancer cells>, Recommanded Product: Ethyl 3-amino-4-(cyclohexylamino)benzoate, the main research area is SLC7A11 anticancer agent breast cancer Lycium; Breast cancer cells; Ferroptosis; Glutathione peroxidase 4 (GPX4); Lycium barbarum polysaccharide; xCT.

Breast cancer is one of the most malignant tumors and is associated with high mortality rates among women. Lycium barbarum polysaccharide (LBP) is an extract from the fruits of the traditional Chinese herb, L. barbarum. LBP is a promising anticancer drug, due to its high activity and low toxicity. Although it has anticancer properties, its mechanisms of action have not been fully established. Ferroptosis, which is a novel anticancer strategy, is a cell death mechanism that relies on iron-dependent lipid reactive oxygen species (ROS) accumulation. In this study, human breast cancer cells (Michigan Cancer Foundation-7 (MCF-7) and MD Anderson-Metastatic Breast-231 (MDA-MB-231)) were treated with LBP. LBP inhibited their viability and proliferation in association with high levels of ferroptosis. Therefore, we aimed to ascertain whether LBP reduced cell viability through ferroptosis. We found that the structure and function of mitochondria, lipid peroxidation, and expression of solute carrier family 7 member 11 (SLC7A11, also known as xCT, the light-chain subunit of cystine/glutamate antiporter system Xc-) and glutathione peroxidase 4 (GPX4) were altered by LBP. Moreover, the ferroptosis inhibitor, Ferrostatin-1 (Fer-1), rescued LBP-induced ferroptosis-associated events including reduced cell viability and glutathione (GSH) production, accumulation of intracellular free divalent iron ions and malondialdehyde (MDA), and down-regulation of the expression of xCT and GPX4. Erastin (xCT inhibitor) and RSL3 (GPX4 inhibitor) inhibited the expression of xCT and GPX4, resp., which was lower after the co-treatment of LBP with Erastin and RSL3. These results suggest that LBP effectively prevents breast cancer cell proliferation and promotes ferroptosis via the xCT/GPX4 pathway. Therefore, LBP exhibits novel anticancer properties by triggering ferroptosis, and may be a potential therapeutic option for breast cancer.

Journal of Zhejiang University, Science, B published new progress about Antitumor agents. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Recommanded Product: Ethyl 3-amino-4-(cyclohexylamino)benzoate.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Song, Ji-Xian; An, Ji-Ren; Chen, Qi; Yang, Xin-Yue; Jia, Cui-Ling; Xu, Shan; Zhao, Ya-shuo; Ji, En-Sheng published the artcile< Liraglutide attenuates hepatic iron levels and ferroptosis in db/db mice>, Formula: C15H22N2O2, the main research area is hepatic tissue ferroptosis iron; Liver; ferroptosis; high glucose; iron overload; liraglutide; oxidative stress.

Liver pathol. changes are as high as 21%-78% in diabetic patients, and treatment options are lacking. Liraglutide is a glucagon-like peptide-1 (GLP-1) receptor that is widely used in the clinic and is approved to treat obesity and diabetes. However, the specific protection mechanism needs to be clarified. In the present study, db/db mice were used to simulate Type 2 diabetes mellitus (T2DM), and they were i.p. injected daily with liraglutide (200μg/kg/d) for 5 wk. Hepatic function, pathol. changes, oxidative stress, iron levels, and ferroptosis were evaluated. First, liraglutide decreased serum AST and ALT levels, and suppressed liver fibrosis in db/db mice. Second, liraglutide inhibited the ROS production by upregulating SOD, GSH-PX, and GSH activity as well as by downregulating MDA, 4-HNE, and NOX4 expression in db/db mice. Furthermore, liraglutide attenuated iron deposition by decreasing TfR1 expression and increasing FPN1 expression. At the same time, liraglutide decreased ferroptosis by elevating the expression of SLC7A11 and the Nrf2/HO-1/GPX4 signaling pathway in the livers of db/db mice. In addition, liraglutide decreased the high level of labile iron pools (LIPs) and intracellular lipid ROS induced by high glucose in vitro. Therefore, we speculated that liraglutide played a crucial role in reducing iron accumulation, oxidative damage and ferroptosis in db/db mice.

Bioengineered published new progress about Adipocyte. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Formula: C15H22N2O2.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Qin, Qiyu; Yu, Naiji; Gu, Yuxiang; Ke, Weishaer; Zhang, Qi; Liu, Xin; Wang, Kaijun; Chen, Min published the artcile< Inhibiting multiple forms of cell death optimizes ganglion cells survival after retinal ischemia reperfusion injury>, Product Details of C15H22N2O2, the main research area is necrostatin1 ferrostain1 neuroprotective agent retinal ischemia reperfusion injury.

Progressive retinal ganglion cells (RGCs) death that triggered by retinal ischemia reperfusion (IR), leads to irreversible visual impairment and blindness, but our knowledge of post-IR neuronal death and related mechanisms is limited. In this study, we first demonstrated that apart from necroptosis, which occurs before apoptosis, ferroptosis, which is characterized by iron deposition and lipid peroxidation, is involved in the whole course of retinal IR in mice. Correspondingly, all three types of RGCs death were found in retina samples from human glaucoma donors. Further, inhibitors of apoptosis, necroptosis, and ferroptosis (z-VAD-FMK, Necrostatin-1, and Ferrostatin-1, resp.) all exhibited marked RGC protection against IR both in mice and primary cultured RGCs, with Ferrostatin-1 conferring the best therapeutic effect, suggesting ferroptosis plays a more prominent role in the process of RGC death. We also found that activated microglia, Muller cells, immune responses, and intracellular reactive oxygen species accumulation following IR were significantly mitigated after each inhibitor treatment, albeit to varying degrees. Moreover, Ferrostatin-1 in combination with z-VAD-FMK and Necrostatin-1 prevented IR-induced RGC death better than any inhibitor alone. These findings stand to advance our knowledge of the post-IR RGC death cascade and guide future therapy for RGC protection.

Cell Death & Disease published new progress about Apoptosis. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Product Details of C15H22N2O2.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Feng, Chuchu; Wu, Yu; Chen, Yantao; Xiong, Xilin; Li, Peng; Peng, Xiaomin; Li, Chunmou; Weng, Wenjun; Zhu, Yafeng; Zhou, Dunhua; Li, Yang published the artcile< Arsenic trioxide increases apoptosis of SK-N-BE (2) cells partially by inducing GPX4-mediated ferroptosis>, Application In Synthesis of 347174-05-4, the main research area is arsenic trioxide anticancer agent ferroptosis neuroblastoma; Arsenic trioxide; Ferroptosis; GPX4; Neuroblastoma; Quantitative proteomic analysis.

Neuroblastoma (NB) is the most common extracranial tumor in central nervous system threatening childrens health with limited therapeutic options. Arsenic trioxide (ATO) has been identified the cytotoxicity in NB cells but the potential mechanism remains unclear. In this study, we attempted to obtain some insight into the mechanisms of cell death induced by ATO in NB cells. Proteomic analyses found that ATO can affect the signaling pathway associated with ferroptosis, including the upregulation of iron absorption (FTL, FTH1, HO-1), ferritinophagy (LC3, P62, ATG7, NCOA4) and modifier of glutathione synthesis (GCLM); downregulation of glutamine synthetase (GS) and GPX4, which was the critical inhibitor of ferroptosis. Western blot anal. revealing GPX4 expression in SK-N-BE (2) cells decreased after treatment with ATO (7.3μM), resulting in a loss of GPX4 activity. Furthermore, Ferroptosis inhibitor ferrostatin-1 partially blocked ATO-induced cell death. Our study revealed that ATO may induce ferroptosis in neuroblastoma cell SK-N-BE (2) by facilitating the downregulation of GPX4, ultimately resulting in iron-dependent oxidative death.

Molecular Biology Reports published new progress about Antitumor agents. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Application In Synthesis of 347174-05-4.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Jiang, Jin-Jin; Zhang, Guo-Fu; Zheng, Jia-Yi; Sun, Ji-Hu; Ding, Shi-Bin published the artcile< Targeting mitochondrial ROS-mediated ferroptosis by quercetin alleviates high-fat diet-induced hepatic lipotoxicity>, Electric Literature of 347174-05-4, the main research area is hepatic lipotoxicity quercetin ferroptosis reactive oxygen species hepatocyte; ferroptosis; hepatic lipotoxicity; mitochondrial ROS; nonalcoholic fatty liver disease; quercetin.

The protective effect of quercetin on nonalcoholic fatty liver disease (NAFLD) has been reported, but its mechanism remains poorly understood. Recently, quercetin was reported to be capable of inhibiting ferroptosis, which is a recognized type of regulated cell death. Moreover, hepatic ferroptosis plays an important role in the progression of NAFLD, but exptl. evidence is limited. Hence, our study aimed to investigate the effect of quercetin on hepatic ferroptosis in high-fat diet (HFD)-induced NAFLD and further elucidate the underlying mol. mechanism. C57BL/6J mice were fed either a normal diet (ND), an HFD, or an HFD supplemented with quercetin for 12 wk. Hepatic lipid peroxidation, steatosis, ferroptosis and iron overload were examined In vitro, steatotic L-02 cells was used to study the potential mechanism. We found that the HFD caused lipid peroxidation, lipid accumulation and ferroptosis in the liver, which were rescued by quercetin supplementation. Consistent with the in vivo results, quercetin alleviated lipid droplet accumulation and reduced the levels of lipid reactive oxygen species (ROS) and ferroptosis in steatotic L-02 cells. Using a mitochondrial ROS (MtROS) scavenger (Mito-TEMPO) and ferroptosis specific inhibitor (Fer-1), we found that quercetin remarkably alleviated lipid droplet accumulation and lipid peroxidation by reducing MtROS-mediated ferroptosis in steatotic L-02 cells. Our data showed that HFD consumption induced lipid accumulation and triggered ferroptosis in liver, ultimately leading to hepatic lipotoxicity, which can be alleviated by quercetin. Findings from this study provide new insight into the mechanism by which quercetin can be used for the prevention and treatment of NAFLD.

Frontiers in Pharmacology published new progress about Bioaccumulation. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Electric Literature of 347174-05-4.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Suzuki-Karasaki, Manami; Ando, Takashi; Ochiai, Yushi; Kawahara, Kenta; Suzuki-Karasaki, Miki; Nakayama, Hideki; Suzuki-Karasaki, Yoshihiro published the artcile< Air Plasma-Activated Medium Evokes a Death-Associated Perinuclear Mitochondrial Clustering>, Safety of Ethyl 3-amino-4-(cyclohexylamino)benzoate, the main research area is air plasma activated medium perinuclear mitochondrial clustering; ROS; cancer; cell death; lipid peroxidation; mitochondrial network; mitochondrial positioning; perinuclear mitochondrial clustering; plasma-activated medium.

Intractable cancers such as osteosarcoma (OS) and oral cancer (OC) are highly refractory, recurrent, and metastatic once developed, and their prognosis is still disappointing. Tumor-targeted therapy, which eliminates cancers effectively and safely, is the current clin. choice. Since aggressive tumors are substantially resistant to multidisciplinary therapies that target apoptosis, tumor-specific activation of another cell death modality is a promising avenue for meeting this goal. Here, we report that a cold atm. air plasma-activated medium (APAM) can kill OS and OC by causing a unique mitochondrial clustering. This event was named monopolar perinuclear mitochondrial clustering (MPMC) based on its characteristic unipolar mitochondrial perinuclear accumulation. The APAM caused apoptotic and nonapoptotic cell death. The APAM increased mitochondrial ROS (mROS) and cell death, and the antioxidants such as N-acetylcysteine (NAC) prevented them. MPMC occurred following mitochondrial fragmentation, which coincided with nuclear damages. MPMC was accompanied by mitochondrial lipid peroxide (mLPO) accumulation and prevented by NAC, Ferrostatin-1, and Nocodazole. In contrast, the APAM induced minimal cell death, mROS generation, mLPO accumulation, and MPMC in fibroblasts. These results suggest that MPMC occurs in a tumor-specific manner via mitochondrial oxidative stress and microtubule-driven mitochondrial motility. MPMC induction might serve as a promising target for exerting tumor-specific cytotoxicity.

International Journal of Molecular Sciences published new progress about Air (plasma-activated medium). 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Safety of Ethyl 3-amino-4-(cyclohexylamino)benzoate.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Kitabayashi, Nanako; Nakao, Shohei; Mita, Yuichiro; Arisawa, Kotoko; Hoshi, Takayuki; Toyama, Takashi; Ishii, Kiyo-aki; Takamura, Toshinari; Noguchi, Noriko; Saito, Yoshiro published the artcile< Role of selenoprotein P expression in the function of pancreatic �cells: Prevention of ferroptosis-like cell death and stress-induced nascent granule degradation>, Product Details of C15H22N2O2, the main research area is pancreatic beta cells ferroptosis cell death; Ferroptosis; GPX4; Pancreatic �cells; Selenoprotein K; Selenoprotein P; Stress-induced nascent granule degradation (SINGD).

Selenoprotein P (SELENOP) is a major selenium (Se)-containing protein (selenoprotein) in human plasma that is mainly synthesized in the liver. SELENOP transports Se to the cells, while SELENOP synthesized in peripheral tissues is incorporated in a paracrine/autocrine manner to maintain the levels of cellular selenoproteins, called the SELENOP cycle. Pancreatic �cells, responsible for the synthesis and secretion of insulin, are known to express SELENOP. Here, using MIN6 cells as a mouse model for pancreatic �cells and Selenop small interfering (si)RNA, we found that Selenop gene knockdown (KD) resulted in decreased cell viability, cellular pro/insulin levels, insulin secretion, and levels of several cellular selenoproteins, including glutathione peroxidase 4 (Gpx4) and selenoprotein K (Selenok). These dysfunctions induced by Selenop siRNA were recovered by the addition of Se. Ferroptosis-like cell death, regulated by Gpx4, was involved in the decrease of cell viability by Selenop KD, while stress-induced nascent granule degradation (SINGD), regulated by Selenok, was responsible for the decrease in proinsulin. SINGD was also observed in the pancreatic �cells of Selenop knockout mice. These findings indicate a significant role of SELENOP expression for the function of pancreatic �cells by maintaining the levels of cellular selenoproteins such as GPX4 and SELENOK.

Free Radical Biology & Medicine published new progress about Antioxidants. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Product Details of C15H22N2O2.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Byun, Jun-Kyu; Lee, Seunghyeong; Kang, Gil Won; Lee, Yu Rim; Park, Soo Young; Song, Im-Sook; Yun, Jae Won; Lee, Jaebon; Choi, Yeon-Kyung; Park, Keun-Gyu published the artcile< Macropinocytosis is an alternative pathway of cysteine acquisition and mitigates sorafenib-induced ferroptosis in hepatocellular carcinoma>, Recommanded Product: Ethyl 3-amino-4-(cyclohexylamino)benzoate, the main research area is sorafenib anticancer cysteine acquisition macropinocytosis ferroptosis hepatocellular carcinoma; Ferroptosis; Hepatocellular carcinoma; Macropinocytosis; Sorafenib; Sorafenib resistance.

Macropinocytosis, an important nutrient-scavenging pathway in certain cancer cells, allows cells to compensate for intracellular amino acid deficiency under nutrient-poor conditions. Ferroptosis caused by cysteine depletion plays a pivotal role in sorafenib responses during hepatocellular carcinoma (HCC) therapy. However, it is not known whether macropinocytosis functions as an alternative pathway to acquire cysteine in sorafenib-treated HCC, and whether it subsequently mitigates sorafenib-induced ferroptosis. This study aimed to investigate whether sorafenib drives macropinocytosis induction, and how macropinocytosis confers ferroptosis resistance on HCC cells. Macropinocytosis, both in HCC cells and HCC tissues, was evaluated by measuring TMR-dextran uptake or lysosomal degradation of DQ-BSA, and ferroptosis was evaluated via C11-BODIPY fluorescence and 4-HNE staining. Sorafenib-induced ferroptosis and macropinocytosis were validated in tumor tissues taken from HCC patients who underwent ultrasound-guided needle biopsy. Sorafenib increased macropinocytosis in human HCC specimens and xenografted HCC tissues. Sorafenib-induced mitochondrial dysfunction was responsible for activation of PI3K-RAC1-PAK1 signaling, and amplified macropinocytosis in HCC. Importantly, macropinocytosis prevented sorafenib-induced ferroptosis by replenishing intracellular cysteine that was depleted by sorafenib treatment; this rendered HCC cells resistant to sorafenib. Finally, inhibition of macropinocytosis by amiloride markedly enhanced the anti-tumor effect of sorafenib, and sensitized resistant tumors to sorafenib. In summary, sorafenib induced macropinocytosis, which conferred drug resistance by mitigating sorafenib-induced ferroptosis. Thus, targeting macropinocytosis is a promising therapeutic strategy to facilitate ferroptosis-based therapy for HCC.

Journal of Experimental & Clinical Cancer Research published new progress about Cell division control protein 42 Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Recommanded Product: Ethyl 3-amino-4-(cyclohexylamino)benzoate.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Zhang, Hongbo; Zhuo, Yuzhen; Li, Dihua; Zhang, Lanqiu; Gao, Qiaoying; Yang, Lei; Yuan, Xiangfei published the artcile< Dihydroartemisinin inhibits the growth of pancreatic cells by inducing ferroptosis and activating antitumor immunity>, SDS of cas: 347174-05-4, the main research area is dihydroartemisinin pancreas cell growth ferroptosis antitumor immunity; Dihydroartemisinin; Ferroptosis; M2; MDSCs; NK; NKT; Pancreatic cancer.

Dihydroartemisinin (DHA) exhibits a direct antitumor effect in various tumor models. However, the mechanism of DHA inducing ferroptosis and activating antitumor immunity remains obscure. Therefore, our study was dedicated to investigate the effect of DHA on ferroptosis and tumor microenvironment and elucidate the underlying mol. mechanism. PDAC orthotopic tumor model was used to investigate tumor proliferation and the population of immune cell in vivo, including M2-type macrophages (M2), myeloid-derived suppressor cells (MDSCs), CD4+T cells, CD8+T cells, NK cells and NKT cells. Levels of GPX4, SLC7A11, P53 and ALOX12 were determined by Real-time PCR and Western blot. CCK8 assay was performed to detect cell viability, and the ferroptosis was distinguished by flow cytometry. Our results showed that DHA inhibited pancreatic cancer cell proliferation. In addition, DHA induced cell ferroptosis by up-regulating the expression of P53 and ALOX12, which was blocked by baicalein (a selective ALOX12 inhibitor). However, DHA also up-regulated the expression of GPX4 and SLC7A11. On the other hand, DHA significantly decreased the suppressive expansion of M2 and MDSCs. Moreover, DHA increased the immune cell population of CD8+T cells, NK cells and NKT cells in the tumor tissues of the tumor-bearing mice. Whereas, the DHA treatment did not affect the frequencies of M2, MDSCs, CD4+T, CD8+T, NK and NKT cells in the spleen. Our research provided exptl. evidences on the activity and mechanism of ferroptosis induced by DHA and revealed that DHA regulated tumor local immunosuppressive microenvironment.

European Journal of Pharmacology published new progress about CD4-positive T cell. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, SDS of cas: 347174-05-4.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics

Jiang, Jin-Jin; Zhang, Guo-Fu; Zheng, Jia-Yi; Sun, Ji-Hu; Ding, Shi-Bin published the artcile< Targeting mitochondrial ROS-mediated ferroptosis by quercetin alleviates high-fat diet-induced hepatic lipotoxicity>, Electric Literature of 347174-05-4, the main research area is hepatic lipotoxicity quercetin ferroptosis reactive oxygen species hepatocyte; ferroptosis; hepatic lipotoxicity; mitochondrial ROS; nonalcoholic fatty liver disease; quercetin.

The protective effect of quercetin on nonalcoholic fatty liver disease (NAFLD) has been reported, but its mechanism remains poorly understood. Recently, quercetin was reported to be capable of inhibiting ferroptosis, which is a recognized type of regulated cell death. Moreover, hepatic ferroptosis plays an important role in the progression of NAFLD, but exptl. evidence is limited. Hence, our study aimed to investigate the effect of quercetin on hepatic ferroptosis in high-fat diet (HFD)-induced NAFLD and further elucidate the underlying mol. mechanism. C57BL/6J mice were fed either a normal diet (ND), an HFD, or an HFD supplemented with quercetin for 12 wk. Hepatic lipid peroxidation, steatosis, ferroptosis and iron overload were examined In vitro, steatotic L-02 cells was used to study the potential mechanism. We found that the HFD caused lipid peroxidation, lipid accumulation and ferroptosis in the liver, which were rescued by quercetin supplementation. Consistent with the in vivo results, quercetin alleviated lipid droplet accumulation and reduced the levels of lipid reactive oxygen species (ROS) and ferroptosis in steatotic L-02 cells. Using a mitochondrial ROS (MtROS) scavenger (Mito-TEMPO) and ferroptosis specific inhibitor (Fer-1), we found that quercetin remarkably alleviated lipid droplet accumulation and lipid peroxidation by reducing MtROS-mediated ferroptosis in steatotic L-02 cells. Our data showed that HFD consumption induced lipid accumulation and triggered ferroptosis in liver, ultimately leading to hepatic lipotoxicity, which can be alleviated by quercetin. Findings from this study provide new insight into the mechanism by which quercetin can be used for the prevention and treatment of NAFLD.

Frontiers in Pharmacology published new progress about Bioaccumulation. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Electric Literature of 347174-05-4.

Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics