Related Experiment Video

Updated: Sep 2, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
07:02

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

7.4K

LKB1 inhibits proliferation, metastasis and angiogenesis of thyroid cancer by upregulating SIK1

Bo Kou1, Xin-Di Wang2, Xiao-Peng Sun1,3

  • 1Department of Otorhinolaryngology-Head&Neck Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, China.

Journal of Cancer
|August 1, 2022
PubMed

Insights

Liver kinase B1 (LKB1) suppresses thyroid cancer by inhibiting proliferation, metastasis, and angiogenesis. Upregulation of LKB1, via SIK1, shows therapeutic potential for thyroid cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • Liver kinase B1 (LKB1), a known tumor suppressor, has demonstrated anti-cancer activity across various malignancies.
  • The specific role of LKB1 in thyroid cancer pathogenesis and progression remained largely undetermined.
  • Understanding LKB1's function is crucial for identifying novel therapeutic targets in thyroid cancer.

Purpose of the Study:

  • To investigate the anti-cancer effects of Liver kinase B1 (LKB1) in thyroid cancer.
  • To elucidate the underlying molecular mechanisms by which LKB1 influences thyroid cancer progression.
  • To evaluate the therapeutic potential of LKB1 as a target for thyroid cancer treatment.

Main Methods:

  • Utilized in vitro assays (MTT, colony formation, flow cytometry, western blot, wound healing, transwell, qPCR, HUVEC migration, ELISA, tube formation) to assess LKB1's effects.
  • Constructed stable cell lines with ectopic LKB1 overexpression in thyroid cancer cell lines (TPC-1, BCPAP).
  • Validated findings in vivo using a nude mice xenograft model.

Main Results:

  • LKB1 expression was significantly lower in thyroid cancer tissues and cell lines compared to normal controls.
  • LKB1 overexpression inhibited proliferation, induced apoptosis, suppressed migration and invasion, and reversed epithelial-mesenchymal transition (EMT) in thyroid cancer cells.
  • LKB1 attenuated angiogenesis by reducing HUVEC recruitment, VEGFA expression, and new vessel formation, mediated through SIK1 upregulation.

Conclusions:

  • LKB1 functions as a tumor suppressor in thyroid cancer, inhibiting proliferation, metastasis, and angiogenesis.
  • LKB1 exerts its anti-cancer effects via the upregulation of SIK1, influencing EMT and MET.
  • LKB1 represents a promising therapeutic target for advancing thyroid cancer treatment strategies.
Keywords:
EMTLKB1SIK1angiogenesismetastasisthyroid cancer

More Related Videos

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer06:51

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

18.1K
Induction and Analysis of Epithelial to Mesenchymal Transition10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

35.9K

Related Concept Videos

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...
4.9K
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...
3.9K
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...
3.9K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
9.2K
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
2.7K
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...
6.6K