Only in Titles

Search results for: Apaf1

paperclip

#33574931   2021/01/07 To Up

Luteolin inhibits proliferation, triggers apoptosis and modulates Akt/mTOR and MAP kinase pathways in HeLa cells.

Flavonoids, a subclass of polyphenols, have been shown to be effective against several types of cancer, by decreasing proliferation and inducing apoptosis. Therefore, the aim of the present study was to assess the anti-carcinogenic potential of luteolin on HeLa human cervical cancer cells, through the use of a cell viability assay, DNA fragmentation assay, mitochondrial membrane potential assay, cell cycle analysis using Annexin/PI staining and flow cytometry, gene expression analysis and a protein profiling array. Luteolin treatment exhibited cytotoxicity towards HeLa cells in a dose- and time-dependent manner, and its anti-proliferative properties were confirmed by accumulation of luteolin-treated cells in sub-G phases. Cytotoxicity induced by luteolin treatment resulted in apoptosis, which was mediated through depolarization of the mitochondrial membrane potential and DNA fragmentation. Furthermore, luteolin treatment increased the expression of various proapoptotic genes, including , and and , whereas the expression of anti-apoptotic genes, including and , was decreased. Cell cycle regulatory genes, including and and , were decreased following treatment. Expression of TRAILR2/DR5, TRAILR1/DR4, Fas/TNFRSF6/CD95 and TNFR1/TNFRSF1A, as well as pro-apoptotic proteins, including BAD, BAX and Cytochrome C were consistently increased, and the expression of antiapoptotic proteins, HIF1α, BCL-X, MCL1 and BCL2, were found to be decreased following treatment. Expression of and and was significantly decreased at the transcriptional level. Expression of GSK3b (p-ser9), PRAS 40 (p-Ther246), BAD (p-ser112), PTEN (p-ser380), AKT (p-ser473), ERK2 (p-Y185/Y187), RISK2 (p-ser386), P70S6k (p-Thr421/ser424), PDK1(p-ser241), ERK1 (p-T202/Y204) and MTOR (p-ser2448) was downregulated and expression of P53 (p-ser241) and P27(p-Thr198) was upregulated by luteolin in a dose-dependent manner, indicating its anti-proliferative and apoptosis enabling properties, and this may have been mediated via inhibition of the AKT and the MAPK pathways.
Ritu Raina, Sreepoorna Pramodh, Naushad Rais, Shafiul Haque, Jasmin Shafarin, Khuloud Bajbouj, Mawieh Hamad, Arif Hussain

1635 related Products with: Luteolin inhibits proliferation, triggers apoptosis and modulates Akt/mTOR and MAP kinase pathways in HeLa cells.

100ug5 mg25 mg96 tests200ug1 Set1 Set200 1000 tests1 Set1 Set1 Set

Related Pathways

paperclip

#33531871   2021/01/04 To Up

A preliminary study: is fibulin 1 a friend or an enemy that needs to be silenced with siRNAs for mesothelioma?

The impaired balance between cell proliferation and cell death, followed the inability to receive the death signals, cells push towards the neoplasia pathway. Fibulin 1 (FBLN1) plays a role as a co-factor in the mechanism of action of a protease such as a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS-1), which has important roles in angiogenesis, can also act as both tumor suppressor gene (TSG) and an oncogene in the main constituent of the extra-cellular matrix. This preliminary study has investigated the effects of silencing FBLN1 with siRNA on autophagy, proliferation, apoptosis pathways in the MSM cell line.
Asude Aksoy, Ahmet Tektemur, Elif Melek, Mustafa Kayfeci, Muhammed F Uslu, Ugurcan Cosar, Ebru Onalan

1810 related Products with: A preliminary study: is fibulin 1 a friend or an enemy that needs to be silenced with siRNAs for mesothelioma?

100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized

Related Pathways

paperclip

#33509203   2021/01/28 To Up

Chromatin conformation changes in peripheral blood can detect prostate cancer and stratify disease risk groups.

Current diagnostic blood tests for prostate cancer (PCa) are unreliable for the early stage disease, resulting in numerous unnecessary prostate biopsies in men with benign disease and false reassurance of negative biopsies in men with PCa. Predicting the risk of PCa is pivotal for making an informed decision on treatment options as the 5-year survival rate in the low-risk group is more than 95% and most men would benefit from surveillance rather than active treatment. Three-dimensional genome architecture and chromosome structures undergo early changes during tumourigenesis both in tumour and in circulating cells and can serve as a disease biomarker.
Heba Alshaker, Robert Mills, Ewan Hunter, Matthew Salter, Aroul Ramadass, Benjamin Matthew Skinner, Willem Westra, Jayne Green, Alexandre Akoulitchev, Mathias Winkler, Dmitri Pchejetski

2839 related Products with: Chromatin conformation changes in peripheral blood can detect prostate cancer and stratify disease risk groups.



Related Pathways

paperclip

#33477797   2021/01/19 To Up

Effects of Deformed Wing Virus Infection on Expressions of Immune- and Apoptosis-Related Genes in Western Honeybees ().

Honeybees are globally threatened by several pathogens, especially deformed wing virus (DWV), as the presence of DWV in western honeybees is indicative of colony loss. The high mortality rate is further exacerbated by the lack of effective treatment, and therefore understanding the immune and apoptosis responses could pave an avenue for the treatment method. In this study, DWV was directly injected into the white-eyed pupae stage of western honeybees (). The DWV loads and selected gene responses were monitored using the real-time PCR technique. The results showed that honeybee pupae that were injected with the highest concentration of viral loads showed a significantly higher mortality rate than the control groups. Deformed wings could be observed in newly emerged adult bees when the infected bees harbored high levels of viral loads. However, the numbers of viral loads in both normal and crippled wing groups were not significantly different. DWV-injected honeybee pupae with 10 and 10 copy numbers per bee groups showed similar viral loads after 48 h until newly emerged adult bees. Levels of gene expression including immune genes (, and ) and apoptosis genes ( and ) were analyzed after DWV infection. The expressions of immune and apoptosis genes were significantly different in infected bees compared to those of the control groups. In the pupae stage, the immune genes were activated by injecting DWV ( and ) or ( and ), a positive control. On the contrary, the expression of apoptosis-related genes (, , , and genes) was suppressed at 96 h post-infection. In DWV-infected newly emerged adult bees, , and genes were upregulated. However, these genes were not significantly different between the normal and crippled wing bees. Our results suggested that DWV could activate the humoral immunity in honeybees and that honeybee hosts may be able to protect themselves from the virus infection through immune responses. Apoptosis gene expressions were upregulated in newly emerged adult bees by the virus, however, they were downregulated during the initial phase of viral infection.
Wannapha Mookhploy, Sasiprapa Krongdang, Panuwan Chantawannakul

1149 related Products with: Effects of Deformed Wing Virus Infection on Expressions of Immune- and Apoptosis-Related Genes in Western Honeybees ().

2 Pieces/Box2 Pieces/Box100100 50 ug5ug2 96T1 mg50 1 mg100 ug

Related Pathways

paperclip

#33469684   2021/01/15 To Up

Total flavone extract from Ampelopsis megalophylla induces apoptosis in the MCF‑7 cell line.

Ampelopsis megalophylla has been found to demonstrate anticancer activities in human cancer cells; however, the effect of total flavone extract (TFE), commonly used in Traditional Chinese Medicine, remains unclear. Furthermore, there is limited information on its effects on breast cancer cell lines. The present study aimed to investigate the inhibitory effects of TFE in different human cancer cell lines. In addition, the underlying mechanisms and the signaling pathways involved were also investigated by determining tumor cell morphological changes, and differences in the cell cycle, apoptosis, mitochondrial transmembrane potential, and related protein expression levels in a breast cancer cell line. It was found that TFE inhibited proliferation in seven cancer cell lines (HeLa, A549, MCF‑7, HepG2, A2780, SW620 and MDA‑MB‑231 and demonstrated a strong inhibitory effect on MCF‑7 cell proliferation. Cell morphological changes were also observed and arrested at the G2/M phase following treatment with TFE at different concentrations. In addition, TFE disrupted the mitochondrial membrane potential and upregulated the expression level of apoptotic proteins, including caspase‑3, ‑8 and ‑9, the Bax/Bcl‑2 ratio, and Apaf‑1 in time‑dependent manner. These results indicated that TFE induced apoptosis of the MCF‑7 cells via a mitochondrial‑mediated apoptotic pathway. In conclusion, TFE is potentially effective in treating breast cancer.
Chun Gui, Chao Zhang, Xiaomei Xiong, Jing Huang, Juan Xi, Ling Gong, Bisheng Huang, Xiuqiao Zhang

1865 related Products with: Total flavone extract from Ampelopsis megalophylla induces apoptosis in the MCF‑7 cell line.

1 mL400 ug1 kit1 mL400 ug1 kit100 extractions1 mg1 mg

Related Pathways

paperclip

#33346776   2020/12/21 To Up

Temporal gene expression profiling of maslinic acid-treated Raji cells.

Maslinic acid is a novel phytochemical reported to target multiple signaling pathways. A complete gene expression profile was therefore constructed to illustrate the anti-tumourigenesis effects of maslinic acid in Raji cells across five time-points. Microarray analysis was used to identify genes that were differentially expressed in maslinic acid treated Raji cells at 0, 4, 8, 12, 24 and 48 h. Extracted RNA was hybridized using the AffymetrixGeneChip to obtain expression profiles. A total of 109 genes were found to be significantly expressed over a period of 48 hours. By 12 hours, maslinic acid regulates the majority of genes involved in the cell cycle, p53 and NF-κB signaling pathways. At the same time, XAF1, APAF1, SESN3, and TP53BP2 were evidently up-regulated, while oncogenes, FAIM, CD27, and RRM2B, were down-regulated by at least 2-fold. In conclusion, maslinic acid shows an hourly progression of gene expression in Raji cells.
Wai Meng Lau, Menaga Subramaniam, Hoe Han Goh, Yang Mooi Lim

2099 related Products with: Temporal gene expression profiling of maslinic acid-treated Raji cells.

300 units4

Related Pathways

paperclip

#33331417   2020/12/18 To Up

Melittin suppresses growth and induces apoptosis of non-small-cell lung cancer cells via down-regulation of TGF-β-mediated ERK signal pathway.

The purpose of this study was to investigate the anti-cancer effect of melittin on growth, migration, invasion, and apoptosis of non-small-cell lung cancer (NSCLC) cells. This study also explored the potential anti-cancer mechanism of melittin in NSCLC cells. The results demonstrated that melittin suppressed growth, migration, and invasion, and induced apoptosis of NSCLC cells in vitro. Melittin increased pro-apoptotic caspase-3 and Apaf-1 gene expression. Melittin inhibited tumor growth factor (TGF)-β expression and phosphorylated ERK/total ERK (pERK/tERK) in NSCLC cells. However, TGF-β overexpression (pTGF-β) abolished melittin-decreased TGF-β expression and pERK/tERK in NSCLC cells. Treatment with melittin suppressed tumor growth and prolonged mouse survival during the 120-day observation in vivo. Treatment with melittin increased TUNEL-positive cells and decreased expression levels of TGF-β and ERK in tumor tissue compared to the control group. In conclusion, the findings of this study indicated that melittin inhibited growth, migration, and invasion, and induced apoptosis of NSCLC cells through down-regulation of TGF-β-mediated ERK signaling pathway, suggesting melittin may be a promising anti-cancer agent for NSCLC therapy.
Renzhi Yu, Miao Wang, Minghuan Wang, Lei Han

1721 related Products with: Melittin suppresses growth and induces apoptosis of non-small-cell lung cancer cells via down-regulation of TGF-β-mediated ERK signal pathway.

1.5 x 10^6 cells5 x 50 ug1.5x10(6) cells50 ug2 Pieces/Box100 ug/vial1 vial

Related Pathways

paperclip

#33178586   2020/10/16 To Up

The Anti-tumor Effects of Coumaric Acid on Melanoma A375 and B16 Cells.

Existing research shows that coumaric acid (CA) can inhibit the proliferation of a variety of tumor cells . However, there are no reports on the anti-tumor effects of CA on melanoma cells. In this study, the inhibitory effects of CA on mouse melanoma B16 and human melanoma A375 cells are reported, and the related mechanisms are investigated. CCK-8 assay was used to detect the effects of CA on cell vitality, colony formation assay was used to observe the effects on cell proliferation, Hoechst 33,258 staining was used to observe the morphology of apoptotic cells, flow cytometry was used to detect the effects on apoptosis and the cell cycle, and western blot was used to measure the levels of cell cycle- and apoptosis-related signaling pathway proteins. CA significantly inhibits cell proliferation of A375 and B16 cells in a dose-dependent manner and obviously induced cell morphological changes. CA arrested A375 cells in the S phase by downregulating the cell cycle-related proteins Cyclin A and CDK2, and arrested B16 cells in the G0-G1 phase through downregulating the cell cycle-related proteins Cyclin E and CDK2. In addition, CA significantly promoted apoptosis of A375 and B16 cells. Furthermore, CA significantly upregulated the levels of Apaf1 and Bax and downregulated the levels of Bcl-2, and subsequently increased the levels of cytoplasmic cytochrome c (Cyto-c), cleaved caspase-3, and cleaved caspase-9, leading to apoptosis in A375 and B16 cells. CA can significantly inhibit the proliferation of human and mouse melanoma cells . Our research is a step in the development of anti-melanoma drugs.
Xue Hu, Zihui Yang, Wenjing Liu, Zhaohai Pan, Xin Zhang, Minjing Li, Xiaona Liu, Qiusheng Zheng, Defang Li

1979 related Products with: The Anti-tumor Effects of Coumaric Acid on Melanoma A375 and B16 Cells.

100ug Lyophilized100 µg100ug Lyophilized200 0.5 ml100ug Lyophilized100ug Lyophilized100ug200

Related Pathways

paperclip

#33177505   2020/11/11 To Up

EMC6 regulates acinar apoptosis via APAF1 in acute and chronic pancreatitis.

Treatment of acute pancreatitis (AP) and chronic pancreatitis (CP) remains problematic due to a lack of knowledge about disease-specific regulatory targets and mechanisms. The purpose of this study was to screen proteins related to endoplasmic reticulum (ER) stress and apoptosis pathways that may play a role in pancreatitis. Human pancreatic tissues including AP, CP, and healthy volunteers were collected during surgery. Humanized PRSS1 (protease serine 1) transgenic (PRSS1) mice were constructed and treated with caerulein to mimic the development of human AP and CP. Potential regulatory proteins in pancreatitis were identified by proteomic screen using pancreatic tissues of PRSS1 AP mice. Adenoviral shRNA-mediated knockdown of identified proteins, followed by functional assays was performed to validate their roles. Functional analyses included transmission electron microscopy for ultrastructural analysis; qRT-PCR, western blotting, co-immunoprecipitation, immunohistochemistry, and immunofluorescence for assessment of gene or protein expression, and TUNEL assays for assessment of acinar cell apoptosis. Humanized PRSS1 mice could mimic the development of human pancreatic inflammatory diseases. EMC6 and APAF1 were identified as potential regulatory molecules in AP and CP models by proteomic analysis. Both EMC6 and APAF1 regulated apoptosis and inflammatory injury in pancreatic inflammatory diseases. Moreover, APAF1 was regulated by EMC6, induced apoptosis to injure acinar cells and promoted inflammation. In the progression of pancreatitis, EMC6 was activated and then upregulated APAF1 to induce acinar cell apoptosis and inflammatory injury. These findings suggest that EMC6 may be a new therapeutic target for the treatment of pancreatic inflammatory diseases.
Jie-Hui Tan, Rong-Chang Cao, Lei Zhou, Zhi-Tao Zhou, Huo-Ji Chen, Jia Xu, Xue-Mei Chen, Yang-Chen Jin, Jia-Yu Lin, Zhao-Chang Qi, Jun-Ling Zeng, Shu-Ji Li, Min Luo, Guo-Dong Hu, Jin Jin, Guo-Wei Zhang

1799 related Products with: EMC6 regulates acinar apoptosis via APAF1 in acute and chronic pancreatitis.

100 ug2 Pieces/Box100ug Lyophilized100ug Lyophilized100ug Lyophilized100 ug100ug Lyophilized100 ug2 Pieces/Box100ug Lyophilized100ug Lyophilized100

Related Pathways

paperclip

#33162824   2020/10/19 To Up

Histone deacetylase inhibitor MPT0B291 suppresses Glioma Growth and partially through acetylation of p53.

Histone deacetylase (HDAC) inhibitors have emerged as a new class of anti-tumor agents for various types of tumors, including glioblastoma. We found that a novel HDAC inhibitor, MPT0B291, significantly reduced the cell viability and increased cell death of human and rat glioma cell lines, but not in normal astrocytes. We also demonstrated that MPT0B291 suppressed proliferation by inducing G1 phase cell cycle arrest and increased apoptosis in human and rat glioma cell lines by flow cytometry and immunocytochemistry. We further investigated the anti-tumor effects of MPT0B291 in xenograft (mouse) and allograft (rat) models. The IVIS200 images and histological analysis indicated MPT0B291 (25 mg/kg, ) reduced tumor volume. Mechanistically, MPT0B291 increased phosphorylation and acetylation/activation of p53 and increased mRNA levels of the apoptosis related genes PUMA, Bax, and Apaf1 as well as increased protein level of PUMA, Apaf1 in C6 cell line. The expression of cell cycle related gene p21 was also increased and Cdk2, Cdk4 were decreased by MPT0B291. Our study highlights the anti-tumor efficacy of a novel compound MPT0B291 on glioma growth.
Batsaikhan Buyandelger, Eli E Bar, Kuo-Sheng Hung, Ruei-Ming Chen, Yung-Hsiao Chiang, Jing-Ping Liou, Huei-Mei Huang, Jia-Yi Wang

2997 related Products with: Histone deacetylase inhibitor MPT0B291 suppresses Glioma Growth and partially through acetylation of p53.

48 assays 5mg10mg5mg10mg50mg

Related Pathways