Related Experiment Video

Updated: Feb 13, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

960

INPP4B restrains cell proliferation and metastasis via regulation of the PI3K/AKT/SGK pathway

Ying Chen1, Zeyu Sun1, Mei Qi1

  • 1Department of Pathogenic Biology, Key Laboratory of Infection and Immunity of Shandong Province, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, China.

Journal of Cellular and Molecular Medicine
|March 9, 2018
PubMed

Insights

Inositol polyphosphate 4-phosphatase type II (INPP4B) acts as a tumor suppressor in cervical cancer. Overexpressing INPP4B inhibits cancer cell proliferation and invasiveness by downregulating the PI3K/AKT pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Cervical cancer is a prevalent gynaecologic malignancy globally.
  • The phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway is frequently activated in cervical cancer.
  • Inositol polyphosphate 4-phosphatase type II (INPP4B) negatively regulates the PI3K/AKT pathway, but its role in cervical cancer is unclear.

Purpose of the Study:

  • To investigate the function of INPP4B in cervical cancer.
  • To determine the impact of INPP4B on cervical cancer cell behavior and the PI3K/AKT pathway.

Main Methods:

  • Overexpression of INPP4B in cervical cancer cell lines (HeLa, SiHa, C33a).
  • Assays for cell proliferation, metastasis, and invasiveness (CCK-8, colony formation, soft agar, Transwell).
  • Western blot analysis to assess protein expression in the PI3K/AKT/SGK3 pathway.
  • Xenograft tumor growth assay in nude mice.
  • Analysis of INPP4B expression in human cervical carcinoma samples.

Main Results:

  • INPP4B overexpression inhibited cervical cancer cell proliferation, metastasis, and invasiveness.
  • INPP4B reduced the expression of key proteins in the PI3K/AKT/SGK3 pathway, including p-AKT, p-SGK3, p-mTOR, phospho-p70S6K, and PDK1.
  • Overexpression of INPP4B decreased tumor growth in vivo.
  • Loss of INPP4B expression was observed in over 60% of human cervical carcinoma samples.

Conclusions:

  • INPP4B functions as a tumor suppressor in cervical cancer.
  • INPP4B inhibits cervical cancer cell proliferation and invasiveness by suppressing AKT and SGK3 activation.
  • Reduced INPP4B expression correlates with cervical cancer progression.
Keywords:
AKTINPP4BSGK3cervical cancer

More Related Videos

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment11:13

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment

Published on: June 9, 2023

2.4K
siRNA Screening to Identify Ubiquitin and Ubiquitin-like System Regulators of Biological Pathways in Cultured Mammalian Cells10:43

siRNA Screening to Identify Ubiquitin and Ubiquitin-like System Regulators of Biological Pathways in Cultured Mammalian Cells

Published on: May 24, 2014

11.8K

Related Concept Videos

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...
5.7K
Cells Coordinate Growth and Proliferation02:36

Cells Coordinate Growth and Proliferation

Cell size is a significant factor impacting cellular design, function, and fitness. There exists some internal coordination by which cells double their masses before division, thus, achieving homeostasis. Coordination between cell growth and proliferation depends on the checkpoints in between cell cycle phases. Loss of coordination or failure in the checkpoint mechanism can drive the cell to uncontrolled growth and loss of cellular function. Like dividing cells that coordinate cellular growth,...
5.2K
pH Regulation in Cells01:28

pH Regulation in Cells

pH plays a critical role in maintaining normal cellular activities. It helps maintain the structure and function of various proteins, dictates the charge on cellular membranes, and is crucial for metabolic reactions inside the cell. Moreover, cells use the energy from the proton motive force to generate ATP.
Cytosolic pH
Under physiological conditions, the cytosolic pH is slightly more acidic than the extracellular pH. However, cells must prevent further acidification of their cytosol to...
7.8K
Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
6.6K
GTPases and their Regulation02:14

GTPases and their Regulation

Guanine nucleotide-binding proteins (G-proteins), also known as GTPases, are a superfamily of proteins that regulate many cellular processes, such as cell signaling, vesicular transport, and the regulation of cell shape and motility. Mutation or dysfunction of these proteins can lead to disease. There are around 40,000 known G-proteins that can broadly be classified into two groups ‒  small G-proteins consisting of a single domain and large multi-domain G-proteins.
Large G-proteins,...
9.9K
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...
5.3K