Related Experiment Video

Updated: Mar 24, 2026

Comparing Metastatic Clear Cell Renal Cell Carcinoma Model Established in Mouse Kidney and on Chicken Chorioallantoic Membrane
05:36

Comparing Metastatic Clear Cell Renal Cell Carcinoma Model Established in Mouse Kidney and on Chicken Chorioallantoic Membrane

Published on: February 8, 2020

9.6K

TIKI2 is upregulated and plays an oncogenic role in renal cell carcinoma

Xiaodong Yuan1, Baijun Dong1, Yunze Xu1

  • 1Department of Urology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China.

Oncotarget
|March 5, 2016
PubMed

Insights

TIKI2 is highly expressed in renal cell carcinoma (RCC) and promotes cancer growth. This study shows TIKI2 acts as an oncogene in RCC, independent of Wnt/β-catenin signaling, highlighting its potential as a therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Wnt antagonists are crucial in renal cell carcinoma (RCC).
  • The specific role of TIKI2, a Wnt family negative regulator, in human RCC remains unclear.
  • Understanding TIKI2's function is vital for advancing RCC treatment strategies.

Purpose of the Study:

  • To investigate the expression and function of TIKI2 in human renal cell carcinoma.
  • To determine TIKI2's role in RCC cell proliferation, invasion, and tumor growth.
  • To explore the relationship between TIKI2 and Wnt/β-catenin signaling in RCC.

Main Methods:

  • Quantitative PCR (qPCR) to analyze TIKI2 mRNA levels in RCC tissues and cell lines.
  • In vitro experiments involving TIKI2 knockdown and overexpression in RCC cell lines (769-P and A498).
  • In vivo tumor xenograft models in mice to assess TIKI2's effect on tumor growth.

Main Results:

  • TIKI2 was significantly upregulated in RCC tissues and cell lines compared to normal tissues and HK-2 cells.
  • TIKI2 knockdown inhibited proliferation, invasion, and clone formation in 769-P cells.
  • Ectopic TIKI2 expression enhanced proliferation, invasion, and clone formation in A498 cells, and increased tumor volume in vivo.
  • TIKI2 modulation did not significantly affect Wnt/β-catenin signaling pathways.

Conclusions:

  • TIKI2 is upregulated in renal cell carcinoma and functions as an oncogene.
  • TIKI2 promotes RCC progression through mechanisms independent of the Wnt/β-catenin pathway.
  • TIKI2 represents a potential therapeutic target for renal cell carcinoma.
Keywords:
TIKI2WntWnt antagonistrenal cell carcinomaβ-catenin

More Related Videos

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter11:32

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter

Published on: March 27, 2020

7.5K
Microfluidic Co-culture of Renal Healthy and Tumor Epithelium to Model Kidney Cancer Progression06:29

Microfluidic Co-culture of Renal Healthy and Tumor Epithelium to Model Kidney Cancer Progression

Published on: January 31, 2025

1.3K

Related Concept Videos

mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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.
The mTOR pathway or the...
5.0K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

1.6K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
6.2K
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...
5.4K
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
4.9K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
8.4K