Related Experiment Video

Updated: Jun 10, 2026

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
06:51

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

Published on: July 21, 2018

LAPTM4B: a novel cancer-associated gene motivates multidrug resistance through efflux and activating PI3K/AKT

L Li1, X H Wei, Y P Pan

  • 1Department of Cell Biology, School of Basic Medical Sciences, Peking University, Beijing, China.

Oncogene
|August 17, 2010
PubMed

Insights

Lysosomal protein transmembrane 4 beta (LAPTM4B-35) promotes cancer multidrug resistance by enhancing drug efflux and activating PI3K/AKT signaling. Knockdown of LAPTM4B-35 using RNA interference can reverse these effects, improving chemotherapy efficacy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Lysosomal protein transmembrane 4 beta (LAPTM4B) is a newly identified cancer-associated gene.
  • LAPTM4B-35 protein is upregulated in over 70% of cancers and acts as an independent prognostic factor.
  • Upregulation of LAPTM4B-35 promotes cancer cell proliferation, migration, invasion, and tumorigenesis.

Purpose of the Study:

  • To investigate the role of LAPTM4B-35 in promoting multidrug resistance in cancer cells.
  • To elucidate the mechanisms by which LAPTM4B-35 confers multidrug resistance.
  • To explore the potential of targeting LAPTM4B-35 for enhancing chemotherapy efficacy.

Main Methods:

  • RNA interference (RNAi) was used to knock down LAPTM4B-35 expression.
  • Colocalization and interaction studies were performed to assess LAPTM4B-35's relationship with P-glycoprotein (P-gp).
  • PI3K/AKT signaling pathway activation was analyzed, and specific PI3K inhibitors were used.

Main Results:

  • LAPTM4B-35 upregulation enhances the efflux of various chemotherapeutic drugs, including doxorubicin, paclitaxel, and cisplatin.
  • LAPTM4B-35 colocalizes and interacts with P-gp, facilitating drug efflux.
  • LAPTM4B-35 activates the PI3K/AKT signaling pathway via its PPRP motif, promoting anti-apoptosis.
  • Knockdown of LAPTM4B-35 or inhibition of PI3K eliminates the multidrug resistance phenotype.

Conclusions:

  • LAPTM4B-35 drives cancer multidrug resistance by promoting P-gp-mediated drug efflux and activating PI3K/AKT signaling.
  • Targeting LAPTM4B-35, particularly through RNAi-mediated knockdown, offers a promising strategy to sensitize cancer cells to chemotherapy.
  • These findings suggest a novel approach to increase chemotherapeutic efficacy in various cancers.

More Related Videos

Multiomics Analysis of TMEM200A as a Pan-Cancer Biomarker07:47

Multiomics Analysis of TMEM200A as a Pan-Cancer Biomarker

Published on: September 15, 2023

Exploring the Pharmacological Action and Molecular Mechanism of Salidroside in Inhibiting MCF-7 Cell Proliferation and Migration11:13

Exploring the Pharmacological Action and Molecular Mechanism of Salidroside in Inhibiting MCF-7 Cell Proliferation and Migration

Published on: June 9, 2023

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...
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...
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 rapamycin-insensitive companion...
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 daughter...
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...