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The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
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In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA...
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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Catenins are characterized by multiple binding domains and dynamic structures that allow them to function as linker proteins in cell junction complexes. All catenins, except α-catenin, contain a characteristic protein sequence called the armadillo repeat and are therefore also called armadillo proteins.
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  9. Predictive And Prognostic Markers
  11. Linc01614 Activated By Sp1 Promoted Malignant Behavior Of Triple-negative Breast Cancer Cells Via The Wnt/b-catenin Signaling Pathway.
  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Linc01614 Activated By Sp1 Promoted Malignant Behavior Of Triple-negative Breast Cancer Cells Via The Wnt/b-catenin Signaling Pathway.

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LINC01614 activated by SP1 promoted malignant behavior of triple-negative breast cancer cells via the WNT/b-Catenin signaling pathway.

Tao Chen1, Kenzi Shi2, Shengrong Sun1

  • 1Department of Breast and Thyroid Surgery, Renmin Hospital of Wuhan University, Wuhan, China.

Revista De Investigacion Clinica; Organo Del Hospital De Enfermedades De La Nutricion
|October 17, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

The long non-coding RNA LINC01614, induced by SP1, promotes triple-negative breast cancer (TNBC) cell malignancy. This occurs through the activation of the Wnt/ß-catenin signaling pathway, highlighting a potential therapeutic target.

Keywords:
LINC01614.SP1Transcription factorTriple-negative breast cancer

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The Use of Mouse Mammary Tumor Cells in an In Vitro Invasion Assay as a Measure of Oncogenic Cell Behavior
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Published on: June 12, 2019

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Triple-negative breast cancer (TNBC) is an aggressive subtype with poor prognosis.
  • Long non-coding RNA LINC01614 is a potential biomarker, but its role in TNBC is unclear.

Purpose of the Study:

  • To investigate the effects of LINC01614 on TNBC cell migration, invasion, and epithelial-mesenchymal transition (EMT).
  • To elucidate the underlying mechanism involving SP1 and Wnt/ß-catenin signaling.

Main Methods:

  • Quantitative PCR to measure LINC01614 and SP1 expression.
  • Cell viability, migration, and invasion assays (CCK-8, Transwell, wound healing).
  • Chromatin immunoprecipitation and luciferase assays to confirm SP1-LINC01614 interaction; Western blotting for EMT and Wnt/ß-catenin pathway markers.
Wnt/ß-catenin pathway

Main Results:

  • LINC01614 expression was upregulated in TNBC tissues and cells.
  • LINC01614 knockdown inhibited TNBC cell viability, migration, invasion, and EMT.
  • SP1 directly activated LINC01614 expression, and SP1 overexpression counteracted the inhibitory effects of LINC01614 knockdown.

Conclusions:

  • SP1-induced LINC01614 promotes TNBC cell malignant behaviors.
  • The Wnt/ß-catenin signaling pathway is activated by SP1-LINC01614, contributing to TNBC progression.