Related Experiment Video

Updated: Jun 11, 2025

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
11:44

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis

Published on: March 30, 2019

7.6K

CircLIFRSA/miR-1305/PTEN axis attenuates malignant cellular processes in non-small cell lung cancer by regulating AKT

Meina Jiang1, Huihui Bai1, Shuai Fang1

  • 1Department of Biochemistry and Molecular Biology and Zhejiang Key Laboratory of Pathophysiology, School of Basic Medical Sciences, Health Science Center, Ningbo University, Ningbo, Zhejiang, 315211, China.

Molecular Cancer
|September 28, 2024
PubMed
Abstract

Insights

Circular RNA LIFRSA (circLIFRSA) is downregulated in non-small cell lung cancer (NSCLC), inhibiting tumor growth and promoting apoptosis. circLIFRSA may serve as an early diagnostic biomarker and therapeutic target for NSCLC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Non-small cell lung cancer (NSCLC) often presents at advanced stages, limiting treatment efficacy.
  • The role of the novel circular RNA LIFRSA (circLIFRSA) in NSCLC pathogenesis remains largely unexplored.
  • Investigating circLIFRSA's involvement in the PTEN/AKT pathway is crucial for understanding NSCLC progression.

Purpose of the Study:

  • To investigate the expression and function of circLIFRSA in non-small cell lung cancer (NSCLC).
  • To elucidate the mechanism by which circLIFRSA affects the PTEN/AKT signaling pathway in NSCLC.
  • To evaluate the potential of circLIFRSA as an early diagnostic biomarker and therapeutic target for NSCLC.

Main Methods:

  • Microarray analysis and RT-qPCR were used to determine circLIFRSA expression levels in NSCLC tissues and cells.
  • Cellular assays (MTT, colony formation, flow cytometry) assessed the impact of circLIFRSA on NSCLC cell growth, proliferation, and apoptosis.
  • Western blotting analyzed the expression of PTEN and phosphorylated AKT (pAKT) to understand the molecular mechanism.

Main Results:

  • circLIFRSA expression was significantly downregulated in NSCLC tissues and cells, correlating with clinicopathological features.
  • circLIFRSA overexpression inhibited NSCLC cell proliferation and growth while promoting apoptosis.
  • circLIFRSA attenuated NSCLC malignancy by regulating the miR-1305/PTEN axis and suppressing AKT phosphorylation.

Conclusions:

  • The circLIFRSA/miR-1305/PTEN axis plays a critical role in attenuating NSCLC progression by modulating AKT phosphorylation.
  • circLIFRSA demonstrates potential as a valuable biomarker for early NSCLC diagnosis.
  • circLIFRSA represents a promising therapeutic target for non-small cell lung cancer treatment.
Keywords:
AKT phosphorylationCircular RNALIFRSAMalignant processNon-small cell lung cancermiR-1305

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

1.5K
Network Pharmacology Prediction and Experimental Validation of Trichosanthes-Fritillaria thunbergii Action Mechanism Against Lung Adenocarcinoma13:18

Network Pharmacology Prediction and Experimental Validation of Trichosanthes-Fritillaria thunbergii Action Mechanism Against Lung Adenocarcinoma

Published on: March 3, 2023

1.2K

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...
3.4K
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
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
6.2K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
5.3K
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
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...
4.7K