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Biology subjects

Linares, L. K.

Publications and source records attributed to Linares, L. K..

3 recordsLinked to original sources

MDM2 stabilization of Notch intracellular domain upon DNA damage plays a major role in non-small cell lung carcinoma response to platinum chemotherapy

Despite major advances in lung cancer clinical management, majority of patients suffering non-small cell lung carcinoma (NSCLC) are treated in first line with platinum in combination with immune checkpoint inhibitors. Although platinum compounds normally display an initial therapeutic effect, relapse constitutes a major challenge in the clinical management of NSCLC patients. Therefore, it is fundamental to understand the relapse underlying mechanisms to find new therapeutic opportunities to improve patients survival. Here, we found that different DNA damage inducers increase the protein levels of Notch Intracellular Domain (NICD), i.e., the active form of NOTCH1. Mechanistically, we unveiled that upon platinum treatment, there was a concomitant increase of MDM2 together with NICD, and we also observed an MDM2-mediated ubiquitination and stabilization of NICD. Of note, using patient-derived xenografts displaying intrinsic carboplatin resistance, we demonstrated that the combination of carboplatin with MDM2 and NICD inhibitors increased survival and reduced tumor growth compared with carboplatin in monotherapy. Moreover, in patients with NSCLC who received platinum chemotherapy, MDM2 expression level in the tumor was correlated with poor progression-free survival, further validating MDM2 key role in the response to platinum compounds. Our findings open a therapeutic opportunity for NSCLC patients, the main lung cancer subtype of the leading cause of death by cancer worldwide.

cancer biology↗

A metabolic crosstalk between liposarcoma and muscle sustains tumor growth

Dedifferentiated (DD-LPS) and Well-differentiated (WD-LPS) liposarcoma are characterized by a systematic amplification of the MDM2 oncogene. We recently demonstrated that p53-independent metabolic functions of chromatin-bound MDM2 (C-MDM2) are exacerbated in LPS and mediate an addiction to serine metabolism in order to sustain tumor growth. Here, we show that metabolic cooperation between LPS and distant muscle, which raise serine and glycine blood levels, is essential for LPS tumor growth. By releasing IL-6, tumor influence distant muscle to upregulate their serine synthesis machinery. Blocking IL-6 secretion or treating LPS cells with FDA approved IL-6 inhibitor, decreased serine production and impaired tumor proliferation. These data reveal IL-6 as a central tumorkine in metabolic crosstalk between tissues and identifies IL-6 as a plausible treatment for LPS patients.

cancer biology↗

RIP140 inhibits glycolysis-dependent proliferation of cancer cells by regulating transcriptional crosstalk between hypoxia induced factor and p53

Cancer cells with uncontrolled proliferation preferentially depend on glycolysis to grow, even in the presence of oxygen. The transcriptional co-regulator RIP140 represses the activity of transcription factors that drive cell proliferation and metabolism and plays a role in mammary tumorigenesis. Here we use cell proliferation and metabolic assays to demonstrate that RIP140-deficiency causes a glycolysis-dependent increase in breast tumor growth. We further demonstrate that RIP140 reduces the transcription of the glucose transporter GLUT3 gene, by inhibiting the transcriptional activity of hypoxia inducible factor HIF-2 in cooperation with p53. Interestingly, RIP140 expression was significantly associated with good prognosis only for breast cancer patients with tumors expressing low GLUT3, low HIF-2 and high p53, thus confirming the mechanism of RIP140 anti-tumor activity provided by our experimental data. Overall, our work establishes RIP140 as a critical modulator of the p53/HIF cross-talk to inhibit breast cancer cell glycolysis and proliferation.

cancer biology↗