Jéssica Nascimento

Universidade Federal do Rio Grande do Sul

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Andréia Buffon

Universidade Federal do Rio Grande do Sul

Aline Beckenkamp

Universidade Federal do Rio Grande do Sul

Danielle Bertodo Santana

Universidade Federal do Rio Grande do Sul

Alessandra Nejar Bruno

University of Palermo

Juliano D. Paccez

International Centre for Genetic Engineering and Biotechnology

Luiz F. Zerbini

International Centre for Genetic Engineering and Biotechnology

Diogo André Pilger

Universidade Federal do Rio Grande do Sul

Massimo Loda

Dana-Farber Cancer Institute

Camila da Silveira Mariot

Universidade Federal do Rio Grande do Sul

Ruy Carlos Ruver Beck

Universidade Federal do Rio Grande do Sul

Cooperative Institutions

Universidade Federal do Rio Grande do Sul

Harvard University

Dana-Farber Cancer Institute

Universidade Federal de Ciências da Saúde de Porto Alegre

Beth Israel Deaconess Medical Center

Universidade Federal do Rio Grande

Universidade de São Paulo

Hospital de Clínicas de Porto Alegre

Broad Institute

Brigham and Women's Hospital

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Abstract B208: Reduction in P2X7 receptor expression is a marker of resistance to ATP treatment in human cervical carcinoma cell line.

Molecular Cancer Therapeutics (2013)

Paola de Andrade Mello Eduardo Cremonese Filippi–Chiela Jéssica Nascimento Franciele Kipper Aline Beckenkamp

Abstract Cervical cancer is the third most commonly diagnosed malignancy and the fourth leading cause of cancer death in females worldwide. The high mortality rate is largely due to the lack of effective therapies for eliminating disease in women with high-grade cervical cancer and the lack of response to chemotherapy of inoperable disease. Thus, to understand the mechanisms involved on cervical cancer development and find a molecular target to prevent it is strongly desirable. Until now, researchers show that HPV infection and suppression of cell death mechanisms like apoptosis are the most important factors involving of cervical carcinogenesis. Anyway, the mechanism that leads cells infected by HPV escape to apoptosis remains unknown. A role for purinergic signaling on control of cell growth and death, mainly through P2X7 receptor activation by extracellular ATP, has been described. We hypothesized that a disruption in this signaling could be involved with cervical cancer resistance to apoptosis and development. Previous work, using human carcinoma cell line SiHa, showed that ATP 5mM induces cell death through apoptosis by P2X7 activation. However, the mechanism involved in this cytotoxic effect remained unclear. To answers this question, we investigate the role of P2X7 on ATP induce cell death. We started analyzing P2X7 protein expression in cells resistant to ATP treatment. In this case, SiHa cells were treated with ATP 5mM for 24, 48, and 72h, and the adherent survival cells were removed and analyzed by Western Blot. After, we knockdown P2X7 receptor in SiHa cell line and evaluate this effect on cell viability after ATP treatment. In addition, we studied the mechanistic way involved in this cell death pathway using EGTA and caspase-3 inhibitor previous to ATP treatment. Unexpectedly, SiHa wild type (WT) cells that remained adherent after treatment with ATP showed less expression of P2X7, suggesting a defense way to apoptosis. Corroborating with this, SiHa cells knockdown (KD) for P2X7 showed increased cell viability when compared to SiHa WT and SiHa KD control, after exposure to ATP 5mM for 24, 48, and 72h. The mechanism of ATP induces apoptosis through P2X7 don't seems to be by increase intracellular calcium and caspase-3 activation, but in an independent caspase way. These findings suggest that P2X7 receptor could be involved with death and resistance cell mechanisms, indicating a possible new target on therapeutical research in cervical cancer and on tumor aggressiveness. Citation Information: Mol Cancer Ther 2013;12(11 Suppl):B208. Citation Format: Paola de Andrade Mello, Eduardo Cremonese Filippi-Chiela, Jessica Nascimento, Franciele Cristina Kipper, Aline Beckenkamp, Danielle Bertodo Santana, Alessandra Nejar Bruno, Guido Lenz, Andréia Buffon. Reduction in P2X7 receptor expression is a marker of resistance to ATP treatment in human cervical carcinoma cell line. [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2013 Oct 19-23; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2013;12(11 Suppl):Abstract nr B208.

10.1158/1535-7163.targ-13-b208

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Encapsulation of orlistat in biodegradable polymeric nanocapsules improves its cytotoxic effect against cervical cancer cells

Journal of Drug Delivery Science and Technology (2023)

Jéssica Nascimento Isadora do Canto Olegário Camila da Silveira Mariot Thayse Viana de Oliveira Paula dos Santos Chaves

HeLa

Nanocapsules

10.1016/j.jddst.2023.105086

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Determinação das atividades da adenosina deaminase e DPPIV/CD26 em células de carcinoma cervical humano

Jéssica Nascimento

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PROJETO PARA UMA PRAÇA NO RIO DE JANEIRO

polemica (2015)

Douglas Britto Jéssica Nascimento Glauber Silva Lauria Arian Carvalho Caroline Gioia

10.12957/polemica.2015.19513

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Abstract 3591: Genetic and pharmacological inhibition of fatty acid synthase (FASN) attenuates prostate cancer driven by Pten loss

Cancer Research (2019)

Caroline F. Ribeiro Débora Campanella Bastos Hubert Pakula Thomas U. Ahearn Jéssica Nascimento

Abstract Inactivation of the tumor suppressor gene phosphatase and tensin homologue (PTEN) is a common alteration in prostate cancer, occurring in the majority of metastatic castration-resistant prostate cancer (mCRPC) cases, and is associated with a more aggressive phenotype and worse prognosis. Another hallmark of prostate cancer is the dysregulation of lipid metabolism with overexpression of fatty acid synthase (FASN), the key enzyme in the de novo synthesis of fatty acids. FASN activity is essential for the generation of new cellular membrane lipids and signaling molecules, conferring growth and survival advantages for cells that overexpress it. Increased FASN expression enhances the aggressive phenotype associated with PTEN loss. To study how inhibition of FASN affects prostate carcinogenesis, we developed a mouse model combining prostate-specific homozygous knockout (KO) of Pten and Fasn genes. Deletion of Fasn, Pten or Fasn/Pten was achieved by expressing Cre recombinase under the control of a Probasin promoter, generating different genotypes: PtenloxP/loxPFasnwt/wtCrepos (P-KO), Ptenwt/wtFasnloxP/loxPCrepos (F-KO) and PtenloxP/loxPFasnloxP/loxPCrepos (F/P-dKO). Inhibition of FASN decreased the weight and volume of the ventral and anterior lobes of murine prostate when compared with Pten single KO mice. Histopathological analysis of the tissues also revealed a reduction in reactive stroma in the ventral and anterior lobes of F/P-dKO in comparison to the P-KO group. This phenotype is suggestive of inhibition of microinvasion. To assess whether FASN inhibition impairs cancer aggressiveness, we tested a novel FASN inhibitor compound, IPI-9119 (Infinity Pharmaceuticals), in epithelial cells from prostate of mice heterozygous for Pten loss. Pharmacological inhibition of de novo lipogenesis lead to decreased cell proliferation and reduction in invasion and motility. Finally, combined loss of PTEN with FASN overexpression assessed in 660 prostate cancer patients with 14.2 years of median follow up, was associated with lethality. Taken together, these data suggest that endogenous lipogenesis supports invasion in a PTEN null background. Since de novo lipogenesis contributes to the aggressive phenotype induced by PTEN loss in murine prostate, targeting lipid metabolism may represent an attractive therapeutic strategy in the context of prostate cancer driven by PTEN loss. Citation Format: Caroline F. Ribeiro, Débora C. Bastos, Hubert Pakula, Thomas Ahearn, Jéssica Nascimento, John S. Clohessy, Lorelei Mucci, Silvio M. Zanata, Giorgia Zadra, Massimo Loda. Genetic and pharmacological inhibition of fatty acid synthase (FASN) attenuates prostate cancer driven by Pten loss [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 3591.

Tensin

10.1158/1538-7445.am2019-3591

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Nanocápsulas poliméricas biodegradáveis de orlistate melhoram seu efeito antiproliferativo em células de câncer de colo de útero

Débora Renz Barreto Vianna Jéssica Nascimento Isadora do Canto Olegário Camila da Silveira Mariot Paula dos Santos Chaves

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LEUCEMIA MIELOIDE CRÔNICA REFRATÁRIA – PRESENÇA DE MUTAÇÃO T315I E RESPOSTA A PONATINIBE

Hematology Transfusion and Cell Therapy (2020)

Jéssica Nascimento Malika Nunes Esmeralda Carvalho P.N.R.J. Faria E.D.C. Viana

10.1016/j.htct.2020.10.212

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Adenosine uptake is the major effector of extracellular ATP toxicity in human cervical cancer cells

Molecular Biology of the Cell (2014)

Paola de Andrade Mello Eduardo Cremonese Filippi–Chiela Jéssica Nascimento Aline Beckenkamp Danielle Bertodo Santana

In cervical cancer, HPV infection and disruption of mechanisms involving cell growth, differentiation, and apoptosis are strictly linked with tumor progression and invasion. Tumor microenvironment is ATP and adenosine rich, suggesting a role for purinergic signaling in cancer cell growth and death. Here we investigate the effect of extracellular ATP on human cervical cancer cells. We find that extracellular ATP itself has a small cytotoxic effect, whereas adenosine formed from ATP degradation by ectonucleotidases is the main factor responsible for apoptosis induction. The level of P2 × 7 receptor seemed to define the main cytotoxic mechanism triggered by ATP, since ATP itself eliminated a small subpopulation of cells that express high P2 × 7 levels, probably through its activation. Corroborating these data, blockage or knockdown of P2 × 7 only slightly reduced ATP cytotoxicity. On the other hand, cell viability was almost totally recovered with dipyridamole, an adenosine transporter inhibitor. Moreover, ATP-induced apoptosis and signaling-p53 increase, AMPK activation, and PARP cleavage-as well as autophagy induction were also inhibited by dipyridamole. In addition, inhibition of adenosine conversion into AMP also blocked cell death, indicating that metabolization of intracellular adenosine originating from extracellular ATP is responsible for the main effects of the latter in human cervical cancer cells.

Purinergic Signalling

Adenosine triphosphate

Apyrase

10.1091/mbc.e14-01-0042

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Citations (56)

Abstract A43: Investigation of dipeptidyl peptidase IV/CD26 role in cervical cancer cell lines.

Molecular Cancer Therapeutics (2013)

Andréia Buffon Aline Beckenkamp Danielle Bertodo Santana Jéssica Nascimento Juliano D. Paccez

Abstract Cervical cancer is a common type of cancer in women and an important public health problem, mainly in developing countries. The glycoprotein DPPIV/CD26 is expressed at the membrane of many cells. It is able to inactivate some bioactive peptides and chemokines, thereby regulating cell proliferation and survival, being involved in processes related to cancer. This enzyme is also present in a soluble form (DPPIV/sCD26), in biological fluids. In this study, we evaluated, the expression and enzymatic properties of the DPPIV/CD26 and its relation with tumoral mechanisms in cervical cancer cell lines. The cervical cancer cells exhibit DPPIV/CD26 enzymatic activity in both membrane bound and, its soluble form, which was confirmed by the inhibition of the enzymatic DPPIV/CD26 activity for sitagliptin phosphate. The CD26 mRNA expression was observed in the SiHa and C33A cells, while the HeLa cells showed no transcripts. The DPPIV/CD26 expression was correlated with the enzymatic activity in these cell lines. We also observed a higher migratory capacity of HeLa (cervical cancer cell line that less express CD26) compared to SiHa (cervical cancer cell line that more express CD26), moreover in the presence of the specific inhibitor we observed that SiHa cell line shows an increase in migration, thus confirming a relationship of this enzyme with the migratory ability. Our results show, that cervical cancer cells present DPPIV/CD26 enzymatic activity in both membrane bound form, as in its soluble form, revealing a differential expression as well as its relationship to cell migration and adhesion. Considering that DPPIV/CD26 plays an important role in tumor biology, this protein may become an important therapeutic target although additional work is required to elucidate the molecular mechanisms associated with DPPIV/CD26 in cervical cancer. Citation Information: Mol Cancer Ther 2013;12(11 Suppl):A43. Citation Format: Andréia Buffon, Aline Beckenkamp, Danielle Bertodo Santana, Jéssica Nascimento, Juliano Paccez, Luiz Fernando Zerbini, Márcia Rosangela Wink, Alessandra Nejar Bruno. Investigation of dipeptidyl peptidase IV/CD26 role in cervical cancer cell lines. [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2013 Oct 19-23; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2013;12(11 Suppl):Abstract nr A43.

HeLa

Dipeptidyl peptidase

10.1158/1535-7163.targ-13-a43

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Genetic ablation of FASN attenuates the invasive potential of prostate cancer driven by Pten loss

The Journal of Pathology (2020)

Débora Campanella Bastos Caroline F. Ribeiro Thomas U. Ahearn Jéssica Nascimento Hubert Pakula

Loss of the tumor suppressor gene Pten in murine prostate recapitulates human carcinogenesis and causes stromal proliferation surrounding murine prostate intraepithelial neoplasia (mPIN), which is reactive to microinvasion. In turn, invasion has been shown to be regulated in part by de novo fatty acid synthesis in prostate cancer. We therefore investigated the effects of genetic ablation of Fasn on invasive potential in prostate-specific Pten knockout mice. Combined genetic ablation of Fasn and Pten reduced the weight and volume of all the prostate lobes when compared to single knockouts. The stromal reaction to microinvasion and the cell proliferation that typically occurs in Pten knockout were largely abolished by Fasn knockout. To verify that Fasn knockout indeed results in decreased invasive potential, we show that genetic ablation and pharmacologic inhibition of FASN in prostate cancer cells significantly inhibit cellular motility and invasion. Finally, combined loss of PTEN with FASN overexpression was associated with lethality as assessed in 660 prostate cancer patients with 14.2 years of median follow-up. Taken together, these findings show that de novo lipogenesis contributes to the aggressive phenotype induced by Pten loss in murine prostate and targeting Fasn may reduce the invasive potential of prostate cancer driven by Pten loss. © 2020 The Authors. The Journal of Pathology published by John Wiley & Sons, Ltd. on behalf of The Pathological Society of Great Britain and Ireland.

Knockout mouse

Gene knockout

WWOX

10.1002/path.5587

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Citations (17)