Related Experiment Video

Updated: Nov 19, 2025

Mosaic Zebrafish Transgenesis for Functional Genomic Analysis of Candidate Cooperative Genes in Tumor Pathogenesis
09:45

Mosaic Zebrafish Transgenesis for Functional Genomic Analysis of Candidate Cooperative Genes in Tumor Pathogenesis

Published on: March 31, 2015

11.5K

Aberrantly high activation of a FoxM1-STMN1 axis contributes to progression and tumorigenesis in FoxM1-driven cancers

Jun Liu1,2, Jipeng Li3,4, Ke Wang2

  • 1State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, Fourth Military Medical University, 710032, Xi'an, Shaanxi, China.

Signal Transduction and Targeted Therapy
|February 2, 2021
PubMed

Insights

Fork-head box protein M1 (FoxM1) drives cancer cell proliferation by increasing Stathmin 1 (STMN1) levels transcriptionally. High FoxM1 and STMN1 co-expression predicts poor prognosis in solid tumors, suggesting a key cancer axis.

Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Biology

Background:

  • Fork-head box protein M1 (FoxM1) is a key transcription factor in cancer development.
  • Stathmin 1 (STMN1), a microtubule-binding protein, is implicated in paclitaxel resistance but its role in cancer is unclear.
  • The regulatory mechanisms of FoxM1 and the function of high STMN1 levels in cancer require further elucidation.

Purpose of the Study:

  • To investigate the correlation between FoxM1 and STMN1 expression in various cancers.
  • To elucidate the functional role of the FoxM1-STMN1 axis in cancer cell proliferation and tumorigenesis.
  • To evaluate the prognostic significance of FoxM1 and STMN1 co-expression in solid tumors.

Main Methods:

  • Analysis of public databases and tissue microarrays for FoxM1 and STMN1 expression patterns.
  • Establishment of lentivirus-mediated FoxM1/STMN1-knockdown cell lines.
  • In vitro assays (cell viability, clone formation, soft agar) and in vivo xenograft mouse models.
  • Chromatin immunoprecipitation (ChIP) assay to determine transcriptional regulation.

Main Results:

  • A strong positive correlation was observed between FoxM1 and STMN1 expression across multiple cancer types.
  • FoxM1 promotes cancer cell proliferation by transcriptionally upregulating STMN1.
  • High levels of FoxM1 and STMN1, particularly their co-expression, are significantly associated with poor prognosis in solid tumors.

Conclusions:

  • The FoxM1-STMN1 axis plays a crucial role in promoting cell proliferation and tumorigenesis in hepatocellular carcinoma, gastric cancer, and colorectal cancer.
  • Combined assessment of FoxM1 and STMN1 offers a more precise biomarker for prognostic prediction in solid tumors.
  • Targeting the FoxM1-STMN1 pathway may represent a potential therapeutic strategy for cancer treatment.

More Related Videos

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells09:37

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Published on: August 25, 2021

2.0K
Zebrafish Model of Neuroblastoma Metastasis05:20

Zebrafish Model of Neuroblastoma Metastasis

Published on: March 14, 2021

3.0K

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...
4.1K
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic...
4.9K
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...
4.9K
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
6.9K
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
9.8K
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
13.5K