Cucurbitacin-E Inhibits Multiple Cancer Cells Proliferation Through Attenuation of Wnt/β-Catenin Signaling

2014 ◽  
Vol 29 (5) ◽  
pp. 210-214 ◽  
Author(s):  
Hui Feng ◽  
Li Zang ◽  
Zhen-Xia Zhao ◽  
Quan-Cheng Kan
Keyword(s):  
Cancer Cells ◽  
Multiple Cancer ◽  
Cucurbitacin E

scholarly journals Landscape of Chimeric RNAs in Non-Cancerous Cells

Genes ◽  
2021 ◽  
Vol 12 (4) ◽  
pp. 466
Author(s):  
Chen Chen ◽  
Samuel Haddox ◽  
Yue Tang ◽  
Fujun Qin ◽  
Hui Li
Keyword(s):  
Cancer Cells ◽  
Cell Lines ◽  
Drug Targets ◽  
Neoplastic Cell ◽  
Multiple Cancer ◽  
Chimeric Rnas ◽  
Healthy Donors ◽  
Cancer Types ◽  
Chimeric Rna ◽  
Cancerous Cells

Gene fusions and their products (RNA and protein) have been traditionally recognized as unique features of cancer cells and are used as ideal biomarkers and drug targets for multiple cancer types. However, recent studies have demonstrated that chimeric RNAs generated by intergenic alternative splicing can also be found in normal cells and tissues. In this study, we aim to identify chimeric RNAs in different non-neoplastic cell lines and investigate the landscape and expression of these novel candidate chimeric RNAs. To do so, we used HEK-293T, HUVEC, and LO2 cell lines as models, performed paired-end RNA sequencing, and conducted analyses for chimeric RNA profiles. Several filtering criteria were applied, and the landscape of chimeric RNAs was characterized at multiple levels and from various angles. Further, we experimentally validated 17 chimeric RNAs from different classifications. Finally, we examined a number of validated chimeric RNAs in different cancer and non-cancer cells, including blood from healthy donors, and demonstrated their ubiquitous expression pattern.

scholarly journals The Application of Embelin for Cancer Prevention and Therapy

Molecules ◽  
2018 ◽  
Vol 23 (3) ◽  
pp. 621 ◽  
Author(s):  
Jeong-Hyeon Ko ◽  
Seok-Geun Lee ◽  
Woong Yang ◽  
Jae-Young Um ◽  
Gautam Sethi ◽  
...  
Keyword(s):  
Cell Death ◽  
Cancer Prevention ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Human Cancer ◽  
Biological Properties ◽  
Multiple Cancer ◽  
Stat3 Signaling ◽  
Oncogenic Pathways ◽  
Cell Death Mechanisms

Embelin is a naturally-occurring benzoquinone compound that has been shown to possess many biological properties relevant to human cancer prevention and treatment, and increasing evidence indicates that embelin may modulate various characteristic hallmarks of tumor cells. This review summarizes the information related to the various oncogenic pathways that mediate embelin-induced cell death in multiple cancer cells. The mechanisms of the action of embelin are numerous, and most of them induce apoptotic cell death that may be intrinsic or extrinsic, and modulate the NF-κB, p53, PI3K/AKT, and STAT3 signaling pathways. Embelin also induces autophagy in cancer cells; however, these autophagic cell-death mechanisms of embelin have been less reported than the apoptotic ones. Recently, several autophagy-inducing agents have been used in the treatment of different human cancers, although they require further exploration before being transferred from the bench to the clinic. Therefore, embelin could be used as a potential agent for cancer therapy.

scholarly journals Blocking IL-6/GP130 Signaling Inhibits Cell Viability/Proliferation, Glycolysis, and Colony Forming Activity in Human Pancreatic Cancer Cells

2019 ◽  
Vol 19 (5) ◽  
pp. 417-427 ◽  
Author(s):  
Xiang Chen ◽  
Jilai Tian ◽  
Gloria H. Su ◽  
Jiayuh Lin
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cell Viability ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Human Pancreatic Cancer ◽  
Multiple Cancer ◽  
Pancreatic Cancer Cells ◽  
Stat3 Phosphorylation

Background:Elevated production of the pro-inflammatory cytokine interleukin-6 (IL-6) and dysfunction of IL-6 signaling promotes tumorigenesis and are associated with poor survival outcomes in multiple cancer types. Recent studies showed that the IL-6/GP130/STAT3 signaling pathway plays a pivotal role in pancreatic cancer development and maintenance.Objective:We aim to develop effective treatments through inhibition of IL-6/GP130 signaling in pancreatic cancer.Methods:The effects on cell viability and cell proliferation were measured by MTT and BrdU assays, respectively. The effects on glycolysis was determined by cell-based assays to measure lactate levels. Protein expression changes were evaluated by western blotting and immunoprecipitation. siRNA transfection was used to knock down estrogen receptor α gene expression. Colony forming ability was determined by colony forming cell assay.Results:We demonstrated that IL-6 can induce pancreatic cancer cell viability/proliferation and glycolysis. We also showed that a repurposing FDA-approved drug bazedoxifene could inhibit the IL-6/IL-6R/GP130 complexes. Bazedoxifene also inhibited JAK1 binding to IL-6/IL-6R/GP130 complexes and STAT3 phosphorylation. In addition, bazedoxifene impeded IL-6 mediated cell viability/ proliferation and glycolysis in pancreatic cancer cells. Consistently, other IL-6/GP130 inhibitors SC144 and evista showed similar inhibition of IL-6 stimulated cell viability, cell proliferation and glycolysis. Furthermore, all three IL-6/GP130 inhibitors reduced the colony forming ability in pancreatic cancer cells.Conclusion:Our findings demonstrated that IL-6 stimulates pancreatic cancer cell proliferation, survival and glycolysis, and supported persistent IL-6 signaling is a viable therapeutic target for pancreatic cancer using IL-6/GP130 inhibitors.

Involvement of CD24 in Multiple Cancer Related Pathways Makes It an Interesting New Target for Cancer Therapy

2018 ◽  
Vol 18 (4) ◽  
pp. 328-336 ◽  
Author(s):  
Shirin Eyvazi ◽  
Bahram Kazemi ◽  
Siavoush Dastmalchi ◽  
Mojgan Bandehpour
Keyword(s):  
Cancer Cells ◽  
Signaling Pathways ◽  
Src Kinases ◽  
Invasion And Metastasis ◽  
Multiple Cancer ◽  
Exact Role ◽  
Promote Cell Proliferation ◽  
Downstream Effectors ◽  
Cluster Of Differentiation

CD24 (cluster of differentiation 24) is a small heavy glycosylated protein, which is overexpressed in many cancer and some cancer stem cells and is associated with the development, invasion, and metastasis of cancer cells. The exact role of CD24 in these processes is not fully understood, however, in this article, it has been tried to present a collection of cancer-related mechanisms attributed to CD24. Based on the literature, CD24 dis-regulates different signaling pathways in various cancer cells, including; Src kinases, STAT3, EGFR, Wnt/β-catenin and MAPK. Src kinases play an important role in the signaling pathways which activate p38 MAPK and STAT3 pathways. Akt and ERK are downstream effectors of CD24-activated EGFR, which promote cell proliferation, invasion and metastasis. CD24 increases the expression of HER2 by the activation of NF-κB transcription factor. Moreover, CD24 up-regulates the expression of miR-21 oncomir through the activation of Src kinases. Identification of the details of these pathways and also new pathways will help researchers to explore new CD24 targeted therapies.

scholarly journals Divergent S Phase Checkpoint Activation Arising from Prereplicative Complex Deficiency Controls Cell Survival

2009 ◽  
Vol 20 (17) ◽  
pp. 3953-3964 ◽  
Author(s):  
Eric Lau ◽  
Gary G. Chiang ◽  
Robert T. Abraham ◽  
Wei Jiang
Keyword(s):  
Dna Replication ◽  
Cancer Cells ◽  
S Phase ◽  
Checkpoint Control ◽  
Multiple Cancer ◽  
Checkpoint Activation ◽  
Diploid Cells ◽  
Prereplicative Complex ◽  
Stress Damage ◽  
S Phase Checkpoint

The DNA replication machinery plays additional roles in S phase checkpoint control, although the identities of the replication proteins involved in checkpoint activation remain elusive. Here, we report that depletion of the prereplicative complex (pre-RC) protein Cdc6 causes human nontransformed diploid cells to arrest nonlethally in G1-G1/S and S phase, whereas multiple cancer cell lines undergo G1-G1/S arrest and cell death. These divergent phenotypes are dependent on the activation, or lack thereof, of an ataxia telangiectasia and Rad3-related (ATR)-dependent S phase checkpoint that inhibits replication fork progression. Although pre-RC deficiency induces chromatin structural alterations in both nontransformed and cancer cells that normally lead to ATR checkpoint activation, the sensor mechanisms in cancer cells seem to be compromised such that higher levels of DNA replication stress/damage are required to trigger checkpoint response. Our results suggest that therapy-induced disruption of pre-RC function might exert selective cytotoxic effects on tumor cells in human patients.

scholarly journals A Static Magnetic Field Inhibits the Migration and Telomerase Function of Mouse Breast Cancer Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Zhu Fan ◽  
Pingdong Hu ◽  
Lekang Xiang ◽  
Ying Liu ◽  
Rongqiao He ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Magnetic Field ◽  
Cell Migration ◽  
Cancer Cells ◽  
Static Magnetic Field ◽  
Breast Cancer Cells ◽  
Mitotic Cell ◽  
Therapeutic Modality ◽  
Specific Marker ◽  
Multiple Cancer

Static magnetic field (SMF) has a potential as a cancer therapeutic modality due to its specific inhibitory effects on the proliferation of multiple cancer cells. However, the underlying mechanism remains unclear, and just a few studies have examined the effects of SMF on metastasis, an important concern in cancer treatment. In this study, we evaluated the effects of moderate SMF (~150 mT) on the proliferation and migration of 4T1 breast cancer cells. Our results showed that SMF treatment accelerated cell proliferation but inhibited cell migration. Further, SMF treatment shortened the telomere length, decreased telomerase activity, and inhibited the expression of the cancer-specific marker telomerase reverse transcriptase (TERT), which may be related to expression upregulation of e2f1, a transcription repressor of TERT and positive regulator of the mitotic cell cycle. Our results revealed that SMF repressed both, cell migration and telomerase function. The telomerase network is responsive to SMF and may be involved in SMF-mediated cancer-specific effects; moreover, it may function as a therapeutic target in magnetic therapy of cancers.

scholarly journals Cucurbitacin E induces apoptosis of human prostate cancer cells via cofilin-1 and mTORC1

2017 ◽  
Vol 13 (6) ◽  
pp. 4905-4910 ◽  
Author(s):  
Xiaolong He ◽  
Qi Gao ◽  
Yayong Qiang ◽  
Wei Guo ◽  
Yadong Ma
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Cucurbitacin E

scholarly journals Noncanonical agonist PPARγ ligands modulate the response to DNA damage and sensitize cancer cells to cytotoxic chemotherapy

2018 ◽  
Vol 115 (3) ◽  
pp. 561-566 ◽  
Author(s):  
Melin J. Khandekar ◽  
Alexander S. Banks ◽  
Dina Laznik-Bogoslavski ◽  
James P. White ◽  
Jang Hyun Choi ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Peroxisome Proliferator ◽  
Multiple Cancer ◽  
P53 Signaling ◽  
Response To Chemotherapy ◽  
P53 Response ◽  
Cancer Types ◽  
Agonist Ligands

The peroxisome-proliferator receptor-γ (PPARγ) is expressed in multiple cancer types. Recently, our group has shown that PPARγ is phosphorylated on serine 273 (S273), which selectively modulates the transcriptional program controlled by this protein. PPARγ ligands, including thiazolidinediones (TZDs), block S273 phosphorylation. This activity is chemically separable from the canonical activation of the receptor by agonist ligands and, importantly, these noncanonical agonist ligands do not cause some of the known side effects of TZDs. Here, we show that phosphorylation of S273 of PPARγ occurs in cancer cells on exposure to DNA damaging agents. Blocking this phosphorylation genetically or pharmacologically increases accumulation of DNA damage, resulting in apoptotic cell death. A genetic signature of PPARγ phosphorylation is associated with worse outcomes in response to chemotherapy in human patients. Noncanonical agonist ligands sensitize lung cancer xenografts and genetically induced lung tumors to carboplatin therapy. Moreover, inhibition of this phosphorylation results in deregulation of p53 signaling, and biochemical studies show that PPARγ physically interacts with p53 in a manner dependent on S273 phosphorylation. These data implicate a role for PPARγ in modifying the p53 response to cytotoxic therapy, which can be modulated for therapeutic gain using these compounds.

scholarly journals LINC02418 promotes colon cancer progression by suppressing apoptosis via interaction with miR-34b-5p/BCL2 axis

2020 ◽  
Author(s):  
Jun Tian ◽  
Peng Cui ◽  
Yifei Li ◽  
Xuequan Yao ◽  
Xiaoyu Wu ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Human Colon ◽  
Luciferase Assay ◽  
Colon Cancer Cells ◽  
Multiple Cancer ◽  
Human Colon Cancer ◽  
Prediction Of Prognosis

Abstract Background LncRNAs have been demonstrated to be functional regulators in tumor progression through interaction with various signaling pathways in multiple cancer types. However, the effect of LINC02418 on CRC progression still remains unclear. Methods LncRNA expression profile in CRC tissues was explored by using the TCGA database. The expressional level of LINC02418 in CRC patients was confirmed by qRT-PCR. Kaplan-Meier analyses was used to investigate the correlations between LINC02418 and OS of patients with CRC. After stably transducing sh-LINC02418 and sh-NC into HCT116 and LoVo cells, cell proliferative, migratory and invasive abilities were detected by CCK-8 assay, colony formation assay and trans-well assay, respectively. The binding between LINC02418 and miR-34b-5p, and the interaction between miR-34b-5p and BCL2 were determined by dual-luciferase assay. Western blot experiments were conducted to further explore the effect of miR-34b-5p on BCL2 signaling pathway. Rescue experiments were performed to uncover the role of LINC02418 /miR-34b-5p/ BCL2 axis in CRC progression. Results LINC02418 was upregulated in human colon cancer samples and its high expression correlated with poor prognosis. LINC02418 promoted cancer progression by enhancing tumor growth, cell mobility and invasiveness of colon cancer cells. Additionally, LINC02418 could physically bind to miR-34b-5p and subsequently interact with BCL2 signaling pathway. Down-regulation of LINC02418 reduced cell proliferation, but transfection of miR-34b-5p inhibitor or BCL2 in LINC02418-silenced colon cancer cells significantly promoted cell growth. Conclusions LINC02418 was upregulated in human colon cancer samples and could be used as indicator for prediction of prognosis. LINC02418 acted as a tumor driver by negatively regulating cell apoptosis through LINC02418 /miR-34b-5p/ BCL2 axis and in colorectal cancer.

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