Smoking promotes the progression of bladder cancer through FOXM1/CKAP2L axis
Contact us if these videos are not relevant.
Contact us if these videos are not relevant.
View abstract on PubMed
Summary
This summary is machine-generated.Smoking promotes bladder cancer by upregulating the FOXM1/CKAP2L axis, driving tumor progression through cell cycle regulation. This molecular mechanism clarifies the link between smoking and bladder cancer development.
Area Of Science
- Oncology
- Molecular Biology
- Genetics
Background
- Smoking is a known risk factor for bladder cancer, but the underlying molecular mechanisms are not fully understood.
- Investigating these mechanisms is crucial for developing targeted therapies and prevention strategies.
Purpose Of The Study
- To elucidate the molecular link between smoking and bladder cancer.
- To identify key genes and pathways involved in smoking-induced bladder cancer progression.
Main Methods
- Cross-sectional and Mendelian randomization analyses to assess smoking-bladder cancer relationships.
- Bioinformatics, in vitro (cell proliferation, migration, invasion assays), and in vivo (subcutaneous tumor model) experiments.
- Chromatin immunoprecipitation (ChIP) assay to determine transcription factor binding.
Main Results
- Confirmed a positive association between smoking and bladder cancer.
- Cigarette smoke extract (CSE) promoted bladder cancer cell proliferation and metastasis.
- CKAP2L was identified as a key gene upregulated by CSE, driving proliferation, migration, invasion, and cell cycle progression.
- FOXM1 was found to bind the CKAP2L promoter, indicating its regulatory role.
Conclusions
- Smoking promotes bladder cancer progression by upregulating the FOXM1/CKAP2L axis.
- This axis drives tumor progression via cell cycle regulation.
- The FOXM1/CKAP2L pathway represents a key mechanism linking smoking to bladder cancer progression.
Contact us if these videos are not relevant.
Contact us if these videos are not relevant.
Related Concept Videos
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...
Mice have long served as models for studying human biology and pathology because of their phylogenetic and physiological similarity with humans. They are also easy to maintain and breed in the laboratory, and hence, many inbred strains are now available for research. Studies on mice have contributed immeasurably to our understanding of cancer biology.
The development of transgenic, knockout, and knock-in mice has led to an exponential increase in their use as model organisms in research,...
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...
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...
Several factors can increase the risk of cancer in an individual. About 50% of cancer cases can be prevented by adopting a healthy lifestyle, regular exercise, eating healthy, and following a modest cancer prevention diet. Epidemiological studies have consistently shown that populations with vegetable and fruit-rich diets have reduced the incidence of cancer. On the other hand, populations who have a diet rich in animal fat, red meat, junk food, or high calories are predisposed to cancer.
Some...
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...