Karolina Weiner-Gorzel. Riona Tully. Tumour-infiltrating Gr-1. DNA repair kinetics (γΗ2ΑΧ expression) were similar in all cell lines. Chemoresistance was effectively reversed in the senescent group, compared with the control (Figure S3A-C). myeloid cells antagonize senescence in cancer. Cellular senescence is a complex physiological state whose main feature is proliferative arrest. Understanding how cancer cells overcome chemotherapy-induced cell death is critical in promoting patient survival. Though its expression in glioblastomas is now well-documented, the role of WT1 in these tumors remains poorly defined. spliceosome. BMI1 also has another way to protect cells from senescence and apoptosis though suppressing oxidative and DNA damage stresses . Emerging evidences show that the chemoresistance of CSCs are in part due to the activation of B cell-specific Moloney murine leukemia virus integration site 1 (BMI1), a stem cell factor, and a polycomb group family member. translesion synthesis; Rev1; chemotherapy; senescence; cell death; Mutagenic translesion synthesis (TLS) carried out by REV1 and POLζ (REV3/REV7) allows cells to tolerate DNA damage by bypassing lesions that block normal DNA replication but at the cost of introducing mutations ().In cancer cells, REV1/POLζ-dependent TLS can contribute to intrinsic … In the case of senescence, anti-oxidants such as NAC in combination with standard chemotherapuetics hold potential in eradicating these metabolically active SASP secreting cells, as do the … Unfortunately, little is known about regulators of quiescence. Weizmann Institute of Science, Israel. However, senescence can also have detrimental consequences as the SASP can enhance proliferation of neighboring tumor cells, chemoresistance, and aging. A549-IR3 exhibited higher proliferation ability and radioresistance compared to parental and A549-IR6 cells. Experience in cell culture, manipulating gene expression as well as in classical cell and molecular biology techniques is required. Luke Gubbins. In a seminal paper published by Bhola et al., gene expression analysis of matched pair of 17 pre- and post … It is often accompanied by Aberrant activation of oncogenes or loss of tumour suppressor genes opposes malignant transformation by triggering a stable arrest in cell growth, which is termed cellular senescence. Ultimately, these functions favor tumor initiation, progression, and chemoresistance, at least in part by a concomitant blockade of senescence, differentiation, and apoptosis. 1. It is often accompanied by Ultimately, these functions favor tumor initiation, progression, and chemoresistance, at least in part by a concomitant blockade of senescence, differentiation, and apoptosis. +. Literature reports that NF-kappaB activation contributes to chemoresistance by regulating oncogenic pathways and multi-drug resistance genes, but recent studies on senescence and chemotherapy have suggested that NF-kappaB activation is essential for chemotherapy induced senescence and tumor regression. An outstanding scientist, Monique drove the lab's major findings showing a potential combinatorial clinical strategy targeting senescence/SASP and antimitotic drugs. Platinum-based chemotherapy induces cellular senescence. myeloid cells antagonize senescence in cancer. p21 is a well-established inducer of cell cycle arrest and senescence (14, 15) The induction of senescence hallmarks by Cellular senescence means a non-proliferative but viable cellular physiological state. Breast cancer stem cells (BCSCs) play a vital role in tumor progression and metastasis. Matthew Ho. The transcription factor nuclear factor kappa B (NF-κB) and the long non-coding RNA (lncRNA) HOTAIR (HOX transcript antisense RNA) have diverse functional … Spindle and kinetochore-associated (SKA) family genes are essential for the maintenance of the metaphase plate and spindle checkpoint silencing during mitosis. In this study, we explored MS in the MDA-MB-231 cell line treated with doxorubicin (DOX). Michele Harrison. DNA repair ability, stemness and senescence were comparatively studied. Mitotic slippage (MS), the incomplete mitosis that results in a doubled genome in interphase, is a typical response of TP53-mutant tumors resistant to genotoxic therapy. (A): Pictorial diagram representing role of BMI1 during cellular events associated with the malignant transformation of stem or differentiated cells into cancer stem cells. Senescence is a cellular response that limits the replica-tion of aged or damaged cells. Consistently, senescent astrocytic CRT cells induced by D‑galactose exhibited increases in the levels of IL‑6 and IL‑8 via NF‑κB activation, which are major SASP … (1999). Ovarian cancer is the most deadly of gynecological malignancies. ... HOTAIR has a critical role in cellular senescence and platinum sensitivity. Since chemoresistance appears to be associated with low senescence in PDOs of ovarian cancer, senescent ovarian cancer cells were established for further study. Hypoxia and cancer stem cells (CSCs) contribute to the paclitaxel (PTX) resistance, but the molecular mechanisms are still elusive. Senescence-driven chemoresistance of MPM C Canino et al 3149 Oncogene. The applicant must hold a doctorate in the field of molecular and cellular biology with good knowledge of cellular senescence and/or cancer biology. Major conclusions: Cellular senescence and cytoprotective autophagy are potential mechanisms of chemoresistance in TNBC. Hypoxia-induced resistance to anticancer drugs is associated with decreased senescence and requires hypoxia-inducible factor-1 activity. The polyploid giant cells arise from the cancer cell population mainly due to genotoxic stress caused by chemotherapy and/or radiotherapy. ... • MiR-126 and 149 control cell growth via p21 induction and senescence mechanism. These polyploidized cells display premature senescence and sort the damaged DNA into the cytoplasm. Several natural compounds that activate Nrf2 (nuclear factor erythroid-derived 2-related factor 2) pathway, which is involved in complex cytoprotective responses, have been paradoxically shown to induce cell death or … By virtue of its protumorigenic roles and tumor cell–selective expression, DEK may represent a new class of drug targets and diagnostic markers. A. R. Özeş, D. F. Miller, O. N. Özeş, F. Fang, Y. Liu, D. Matei, T. Huang, K. P. Nephew. John McCaffrey. NF-κB-HOTAIR axis links DNA damage response, chemoresistance and cellular senescence in ovarian cancer. In addition, as of the accumulation of senescent cells, we proposed that the senescence‑associated secretory phenotype (SASP) can stimulate age‑related pathologies and chemoresistance in brain. TMZ resistance is regulated by complex genetic and epigenetic networks. One emerging mechanism of chemoresistance is the tumour cell secretome (TCS), an array of protumorigenic factors released by tumour cells. Nat Med (2005). Hence, a better understanding of the cellular pathways underlying escape from cell death is critical. 4 Remarkably, although mounting evidence has previously demonstrated that senescence induction can be overcome by accumulation of secondary mutations in tumor cells, the possibility that extrinsic factors in the tumor microenvironment … Myeloid Cells Medicine & Life Sciences 93%. the senescence‑associated secretory phenotype (SASP) can stimulate age‑related pathologies and chemoresistance in brain. FoxO3 Inactivation Promotes Human Cholangiocarcinoma Tumorigenesis and Chemoresistance Through Keap1-Nrf2 Signaling Li Guan,1 Lei Zhang,1 Zhicheng Gong,1 Xiaonan Hou,1 Yuxiu Xu,1 Xinhua Feng,2 Hongyang Wang,3 and Han You1 FoxO transcription factors have b een reported to play pivotal roles in tumorigenesi s and drug resistance. The release of extranuclear DNA in senescent cells via polyploidizing MS requires more study … Malignant pleural mesothelioma (MPM) is an asbestos-related cancer arising from mesothelial cells of the pleura. Wilms’ tumor 1 (WT1) is a transcription factor with a multitude of downstream targets that have wide-ranging effects in non-glioma cell lines. Chemoresistance is a major factor driving tumour relapse and the high rates of cancer-related deaths. The findings suggest that an NF-κB-HOTAIR axis drives a positive-feedback loop cascade during DDR and contributes to cellular senescence and chemotherapy resistance in ovarian and other cancers. Musiani et al. chemoresistance in prostate and other cancers. Cellular senescence in stromal cells is one of the reasons for therapeutic resistance in advanced cancer; thus, it is an inevitable phenomenon to address while seeking an effective cancer treatment strategy. promoted chemoresistance through suppression of cell senescence and induction of glucose metabolism in ovarian cancer organoids and cells. ... BMI1 plays a role in cell cycle, cell immortalization, and senescence. These two non-apoptotic outcomes in response to chemotherapy are inextricably linked and are neglected outcomes … Resistance to temozolomide (TMZ), the first-line chemotherapeutic drug for glioblastoma (GBM) and anaplastic gliomas, is one of the most significant obstacles in clinical treatment. The induction of cellular senescence is one mechanism by which this effect may be achieved.1 Cellular senescence is a general program of persis-tent growth arrest in response to sublethal stresses in both normal nontransformed and immortalized transformed cells. We hypothesized that WT1 functions as an oncogene to enhance glioblastoma viability and … Survival of a rare population of tumor cells possessing CSC-like characteristics following chemotherapy is a key contributor of resistance (150–153). In this study, we explored MS in the MDA-MB-231 cell line treated with doxorubicin (DOX). These two non-apoptotic outcomes in response to chemotherapy are inextricably linked and are neglected outcomes … of polyploidy as the third component of the paradoxical senescence–self-renewal duality of the chemoresistance is not su ciently understood [8,26,31–34]. Dive into the research topics of 'Tumor-infiltrating myeloid cells drive senescence evasion and chemoresistance in tumors'. Full PDF Package Download Full PDF Package. Mitotic slippage (MS), the incomplete mitosis that results in a doubled genome in interphase, is a typical response of TP53-mutant tumors resistant to genotoxic therapy. The numerical number given on each arrow within the figure represents the reference number … Aberrant activation of oncogenes or loss of tumour suppressor genes opposes malignant transformation by triggering a stable arrest in cell growth, which is termed cellular senescence. The results showed that a single treatment of PGV-0 induced cellular senescence and increased senescence cells in combination treatment. Senescence is a cellular response that limits the replica-tion of aged or damaged cells. MPM ALDHbright cells exhibit TIC properties To characterize the ALDHbright cell subpopulation induced by p-CM, we FACS-sorted to purify ALDHbright cells and ALDHlow cells from MSTO211H cells, and Huizhen Sun 1*, Husheng Wang 1*, Xue Wang 1*, Yoichi Aoki 2, Xinjing Wang 1, Yufei Yang 3, Xi Cheng 3, Ziliang Wang 1 , Xipeng Wang 1 . BMI1 also has another way to protect cells from senescence and apoptosis though suppressing oxidative and DNA damage stresses [37]. Metabolic Remodeling During Phenotypic Plasticity and Therapy Resistance MicorRNAs (miRNA) have been considered a promising therapeutic strategy in various cancers. The main outputs of senescence are beneficial as senescence imposes a potent barrier to tumorigenesis and contributes to tissue repair and embryonic development. The reactivation of senescence in cancer and the subsequent clearance of senescent cells are suggested as therapeutic intervention in the eradication of cancer. Premature senescence recapitulates cellular and molecular features of replicative senescence (), which is a safeguard program that limits the growth potential, but not necessarily the viability, of a dividing cell as a consequence of the progressive shortening of its telomeres.Senescent cells, arrested in the G1 phase of the cell cycle, typically appear flattened … The numerical number given on each arrow within the figure represents the reference number … Singapore. Major conclusions: Cellular senescence and cytoprotective autophagy are potential mechanisms of chemoresistance in TNBC. 2 was used as a control senescence-inducing agent (Fig. Abstract. The chemoresistance of cancer cells is a multifactorial mechanism in which de-regulated apoptotic pathways, the oxidative response and cancer cell migration play a crucial role. Cellular senescence and cytoprotective autophagy are potential mechanisms of chemoresistance in TNBC. These two non-apoptotic outcomes in response to chemotherapy are inextricably linked and are neglected outcomes of investigation in the chemotherapeutic arena. NF-κB-HOTAIR axis links DNA damage response, chemoresistance and cellular senescence in ovarian cancer. processes implicated in chemoresistance will be helpful for the development of novel treatments. Recent findings indicate that chemoresistance in AML is associated with chemotherapy (Ara-C)-induced senescence (Duy et al., Cancer Discovery 2021). Senescence-Induced Stemness and Its Therapeutic Implication in Cancers Including TNBC. (A): Pictorial diagram representing role of BMI1 during cellular events associated with the malignant transformation of stem or differentiated cells into cancer stem cells. Other projects within the major themes of the lab will also be considered. An overexpression of genes related to inflammation, like MCP-1, IL-15, and TLR4 was found in senescent human dermal fibroblasts, but was absent in senescent retinal pigment epithelial cells and vascular endothelial cells. This indicates that the connection between inflammation and senescence may be cell type specific [ 26 ]. However, therapeutic approaches … These determinants of BCSCs including the plasticity between the mesenchymal and epithelial phenotypes often leads to minimal residual disease (MRD), tumor … CXCR2 promoted anti-apoptosis, anti-senescence, and epithelial-to-mesenchymal transition (EMT) of breast cancer cells, leading to the enhanced metastasis and chemoresistance. secrete IL-6, promoting chemoresistance. Artemin can stimulate radio- and chemoresistance through - upregulating TWIST1 and BMI1 [14]. 753b is a novel BCL-XL/BCL-2 proteolysis targeting chimera (PROTAC) that targets both BCL-XL and BCL-2 to the Von Hippel-Lindau (VHL) E3 ligase, sparing platelets that lack VHL expression. In conclusion, our results implicate overexpression of the 6p pro-oncogene DEK as an extremely frequent event in metastatic melanomas. Remarkably, this single event can have a dual effect on melanoma cell proliferation and chemoresistance (preventing senescence and inducing the antiapoptotic MCL-1, respectively). ... KDM5A has been implicated in senescence pathways, both positively and negatively. Hepatocellular carcinoma (HCC) is one of the most frequent malignant tumors. It is the basis of aging, and it exists in the body at any time point. Bielak-Zmijewska A, Wnuk M, Przybylska D, Grabowska W, Lewinska A, Alster O. et al. I show that P13K/AKT/mTOR signaling is repressed in senescent endothelial cells and serves as switch, turning off chronic senescence-associated IL-6 production. MPM ALDHbright cells exhibit TIC properties To characterize the ALDHbright cell subpopulation induced by p-CM, we FACS-sorted to purify ALDHbright cells and ALDHlow cells from MSTO211H cells, and Amplified in breast cancer 1 enhances human cholangiocarcinoma growth and chemoresistance by simultaneous activation of Akt and ... oxygen consumption or by inhibiting the expression of ROS scavengers such as sestrin 3, 20 which promotes cellular senescence and sensitizes cells to ROS-mediated apoptosis. 1B). 1B). ... Senescent cells demonstrate an increase in senescence-associated β-galactosidase (SABG). siRNA leaded to apoptosis and senescence in tumor cells and increases susceptibility to cytotoxic agents [37, 40]. Fiona Furlong. Role of BMI1 in malignant transformation of stem cells into cancer stem cells and chemoresistance. Therefore, our data suggest that overexpression of H2A.Z isoforms enables cells to overcome the oncoprotective barrier associated with senescence, favoring PDAC tumor grow and chemoresistance. ... Senescent cells demonstrate an increase in senescence-associated β-galactosidase (SABG). In fact, small hairpin RNA-mediated ablation of STAT3 deeply attenuates the induction of EMT genes and the increase of ALDH bright cells induced by SASP-cytokines. Cellular Senescence Medicine & Life Sciences 100%. Importantly, both these cellular fates are induced in tumour hypoxia, a key tumour microenvironment associated with TNBC and integral to chemoresistance. Role of BMI1 in malignant transformation of stem cells into cancer stem cells and chemoresistance. Senescent cells lack the capacity to proliferate, but are known to aggravate tumorigenesis. secrete IL-6, promoting chemoresistance. Matthew Guang. Idiopathic pulmonary fibrosis (IPF) is an interstitial fibrous lung disease with unknown etiology, characterized by irreversible destruction … Cellular senescence has been associated with age-related diseases, wound healing, fibrosis, diabetes and cancer. Senescent cells lack the capacity to proliferate, but are known to aggravate tumorigenesis. The polyploid giant cells arise from the cancer cell population mainly due to genotoxic stress caused by chemotherapy and/or radiotherapy. This study un-veils a physiological switch involving PI3K/AKT/mTOR signaling that restrains the senescence secretory respons-es to limit the detrimental consequences of persistent inflammation. Artemin can stimulate radio- and chemo-resistance through upregulating TWIST1 and BMI1 . These data implicate endothelial paracrine signaling in the promotion of chemoresistance and elucidates the molecular control of acute vs. chronic therapy-induced cytokine secretion. A comparison of replicative senescence and doxorubicin-induced premature senescence of vascular smooth muscle cells … Chemoresistance is a severe clinical challenge in breast cancer. • MiR-126 and 149 promote cell proliferation by suppressing SOX2, NANOG, and Oct4. Recent studies have shown AD induces cellular senescence, a phenomenon that is cell-autonomously tumor-suppressive … p21 is a well-established inducer of cell cycle arrest and senescence (14, 15) The induction of senescence hallmarks by Asia Pacific Geriatrics Conference 2016. MicorRNAs (miRNA) have been considered a promising therapeutic strategy in various cancers. Autophagy-induced senescence and chemoresistance following anti-mitotic therapy (2016). Cell. Essential Qualifications: Recent recipients of PhD or MD/PhD (or equivalent) degree or close to obtaining a doctoral degree. 1.2 Oncogene Unlike tumor suppressor genes, which induces anti-proliferative mechanisms such as senescence and apoptosis, proto-oncogenes are responsible for promoting cellular proliferation and differentiation. Unfortunately, little is known about regulators of quiescence. The fate of chemoresistance in triple negative breast cancer (TNBC) Elma A. O’Reillya,b,⁎, Luke Gubbinsa, Shiva Sharmaa,b, Riona Tullya, Matthew Ho Zhing Guanga, Karolina Weiner-Gorzela,JohnMcCaffreyc, Michele Harrisond, Fiona Furlonge, Malcolm Kellb, Amanda McCanna a UCD Conway Institute of Biomolecular and Biomedical Research, UCD School of Medicine and … TWIST1 and BMI1 expressions in different cancer types with cancer chemoresistance are presented in Table 2. 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