Related Experiment Video

Updated: Jul 3, 2025

Live Cell Imaging of the TGF- β/Smad3 Signaling Pathway In Vitro and In Vivo Using an Adenovirus Reporter System
11:06

Live Cell Imaging of the TGF- β/Smad3 Signaling Pathway In Vitro and In Vivo Using an Adenovirus Reporter System

Published on: July 30, 2018

10.6K

SP3-induced Timeless transcription contributes to cell growth of lung adenocarcinoma cells

Ping Tian1, Dajun Du2, Li Yang3

  • 1Medical School, Xinyang Vocational and Technical College, Xinyang, Henan, China.

Plos One
|February 14, 2024
PubMed
Abstract

Insights

Specificity protein 3 (SP3) upregulates Timeless in lung adenocarcinoma (LUAD), promoting cancer cell proliferation. Targeting the SP3/Timeless axis offers a potential therapeutic strategy for LUAD patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Timeless is implicated in replication checkpoints and human malignancies.
  • The interaction between Specificity protein 3 (SP3) and Timeless in lung adenocarcinoma (LUAD) remains uninvestigated.

Purpose of the Study:

  • To investigate the role of Timeless in LUAD.
  • To explore the regulatory mechanism of Timeless transcription by SP3 in LUAD.

Main Methods:

  • Analysis of Timeless expression and clinical significance in LUAD using TCGA data.
  • Lentivirus-mediated Timeless knockdown in A549 cells to assess proliferation and pemetrexed (PEM) resistance.
  • Identification of transcription factors binding to the Timeless promoter via DNA pull-down and HPLC-MS/MS, followed by KEGG pathway analysis.
  • Dual-luciferase reporter assay to confirm SP3's role in Timeless transcription.

Main Results:

  • Timeless is overexpressed in LUAD and serves as a potential diagnostic/prognostic biomarker.
  • Timeless knockdown reduced LUAD cell viability, proliferation, and sensitized PEM-resistant cells to PEM.
  • SP3 was identified as a transcription factor promoting Timeless transcription through binding to the F2 fragment of its promoter.

Conclusions:

  • SP3-mediated upregulation of Timeless promotes LUAD cell proliferation.
  • The SP3/Timeless axis represents a potential therapeutic target for LUAD.

More Related Videos

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

13.0K
Author Spotlight: Exploring the Role of Inflammation in the Co-occurrence of Primary Sjogren's Syndrome and Lung Adenocarcinoma10:21

Author Spotlight: Exploring the Role of Inflammation in the Co-occurrence of Primary Sjogren's Syndrome and Lung Adenocarcinoma

Published on: September 20, 2024

434

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

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...
4.5K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
7.4K