Related Experiment Video

Updated: Jul 20, 2025

A Guide to Production, Crystallization, and Structure Determination of Human IKK1/α
11:27

A Guide to Production, Crystallization, and Structure Determination of Human IKK1/α

Published on: November 2, 2018

9.2K

Receptor-interacting protein kinase 1 (RIPK1) regulates cervical cancer cells via NF-κB-TNF-α pathway: An in vitro

Wenqi Bai1, Fengjie Cui1, Zihan Wang2

  • 1Departments of Oncology Gynecology, The First Affiliated Hospital of Bengbu Medical College, No. 287 Changhuai Road, Bengbu 233004, China.

Translational Oncology
|July 29, 2023
PubMed
Abstract

Insights

Receptor-interacting protein kinase 1 (RIPK1) is upregulated in cervical cancer (CC), promoting tumor growth and spread. Inhibiting RIPK1 may offer a new therapeutic strategy for CC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Death Signaling

Background:

  • Cervical cancer (CC) presents significant global health challenges.
  • Receptor-interacting protein kinase (RIPK) family members regulate critical cellular processes like inflammation and cell death.
  • The specific role of RIPK1 in CC pathogenesis remains largely undefined.

Purpose of the Study:

  • To investigate the clinical significance and biological functions of RIPK1 in cervical cancer.
  • To explore RIPK1 as a potential therapeutic target for CC treatment.

Main Methods:

  • Analysis of RIPK1 expression in 50 CC patient tissues using immunohistochemistry.
  • In vitro studies including western blotting, CCK-8, colony formation, and wound healing assays.
  • Investigation of RIPK1's regulatory role in NF-κB and TNF signaling pathways.

Main Results:

  • RIPK1 expression is significantly elevated in CC tumor tissues compared to adjacent tissues.
  • Higher RIPK1 levels correlate with a poorer prognosis in CC patients.
  • Silencing RIPK1 suppressed CC cell proliferation, migration, and invasion in vitro.
  • RIPK1 was found to enhance CC cell migration, invasion, and proliferation via regulation of NF-κB and TNF.

Conclusions:

  • RIPK1 plays a crucial role in CC development and progression by promoting cell proliferation and spread while inhibiting apoptosis.
  • RIPK1 activation of NF-κB and regulation of TNF are key mechanisms driving CC.
  • RIPK1 represents a promising molecular target for novel cervical cancer therapies.
Keywords:
ApoptosisCervical carcinomaEceptor-interacting protein kinase 1NF-κBTargeted therapy

More Related Videos

NF-κB-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells10:57

NF-κB-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells

Published on: January 12, 2020

10.6K
Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion09:23

Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion

Published on: April 2, 2020

6.5K

Related Concept Videos

NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
7.5K
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...
2.1K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
4.8K
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...
4.6K
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...
3.8K
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...
3.7K