Publications by authors named "Emanuel Jeldes"

Astrogliosis is a process by which astrocytes, when exposed to inflammation, exhibit hypertrophy, motility, and elevated expression of reactivity markers such as Glial Fibrillar Acidic Protein, Vimentin, and Connexin43. Since 1999, our laboratory in Chile has been studying molecular signaling pathways associated with "gliosis" and has reported that reactive astrocytes upregulate Syndecan 4 and αβ Integrin, which are receptors for the neuronal glycoprotein Thy-1. Thy-1 engagement stimulates adhesion and migration of reactive astrocytes and induces neurons to retract neurites, thus hindering neuronal network repair.

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Elevated expression of CAV1 in breast cancer increases tumor progression. Extracellular vesicles (EVs) from CAV1-expressing MDA-MB-231 breast cancer cells contain Tenascin C (TNC), but the relevance of TNC remained to be defined. EVs were characterized by nanotracking analysis, microscopy and western blotting.

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Article Synopsis
  • Breast cancer is the most common cancer among women and a leading cause of cancer-related deaths globally.
  • The study investigates long non-coding mitochondrial RNAs (ncmtRNAs) and how knocking down antisense ncmtRNAs (ASncmtRNAs) selectively induces death in cancer cells without affecting normal cells.
  • Results show that knocking down ASncmtRNAs leads to changes in proteins involved in cell cycle regulation, highlighting a potential strategy for protecting normal cells during cancer treatments while targeting tumors.
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During intercellular communication, cells release extracellular vesicles such as exosomes, which contain proteins, ncRNAs and mRNAs that can influence proliferation and/or trigger apoptosis in recipient cells, and have been proposed to play an essential role in promoting invasion of tumor cells and in the preparation of metastatic niches. Our group proposed the antisense non-coding mitochondrial RNA (ASncmtRNA) as a new target for cancer therapy. ASncmtRNA knockdown using an antisense oligonucleotide (ASO-1537S) causes massive death of tumor cells but not normal cells and strongly reduces metastasis in mice.

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Human and mouse cells display a differential expression pattern of a family of mitochondrial noncoding RNAs (ncmtRNAs), according to proliferative status. Normal proliferating and cancer cells express a sense ncmtRNA (SncmtRNA), which seems to be required for cell proliferation, and two antisense transcripts referred to as ASncmtRNA-1 and -2. Remarkably however, the ASncmtRNAs are downregulated in human and mouse cancer cells, including HeLa and SiHa cells, transformed with HPV-18 and HPV-16, respectively.

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Article Synopsis
  • Knockdown of antisense noncoding mitochondrial RNAs (ASncmtRNAs) causes apoptosis in cancer cells without affecting normal cells, indicating potential for targeted cancer therapy.
  • In vitro studies showed that targeting ASncmtRNAs induces cell death in mouse renal adenocarcinoma cells but spares healthy kidney cells.
  • In vivo experiments demonstrated that treatment with ASncmtRNA knockdown not only inhibited tumor growth and metastasis in a more natural kidney environment but also improved survival rates in mice.
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Hepatocellular carcinoma (HCC) is one of the most commonly diagnosed cancers worldwide. Chemoprevention of HCC can be achieved through the use of natural or synthetic compounds that reverse, suppress or prevent the development of cancer progression. In this study, we investigated the antiproliferative effects and the mechanism of action of two compounds, 2,3,4'-trimethoxy-2'-hydroxy-chalcone (CH1) and 3'-bromo-3,4-dimethoxy-chalcone (CH2), over human hepatoma cells (HepG2 and Huh-7) and cultured mouse hepatocytes (HepM).

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