Deleted in lung and esophageal cancer 1

From WikiMD's Wellness Encyclopedia


Overview[edit | edit source]

Deleted in Lung and Esophageal Cancer 1 (DLEC1) is a tumor suppressor gene located on chromosome 3p22.3. It is implicated in the pathogenesis of lung cancer and esophageal cancer. The gene is often found to be deleted or downregulated in these cancers, suggesting its role in tumor suppression.

Genomic Location and Structure[edit | edit source]

DLEC1 is located on the short arm of chromosome 3, specifically at the 3p22.3 locus. The gene spans approximately 630 kilobases and consists of 37 exons. The protein encoded by DLEC1 is a large protein with multiple domains, which are thought to be involved in its tumor suppressor functions.

Function[edit | edit source]

The exact function of DLEC1 is not fully understood, but it is believed to play a role in regulating cell growth and apoptosis. Studies suggest that DLEC1 may interact with other proteins involved in cell cycle regulation and DNA repair. Its loss or downregulation can lead to uncontrolled cell proliferation, a hallmark of cancer.

Role in Cancer[edit | edit source]

DLEC1 is frequently deleted or epigenetically silenced in non-small cell lung cancer (NSCLC) and esophageal squamous cell carcinoma (ESCC). The loss of DLEC1 expression is associated with poor prognosis and advanced disease stage in these cancers.

Lung Cancer[edit | edit source]

In lung cancer, particularly NSCLC, DLEC1 is often found to be deleted or methylated, leading to its inactivation. Restoration of DLEC1 expression in lung cancer cell lines has been shown to inhibit cell growth and induce apoptosis, supporting its role as a tumor suppressor.

Esophageal Cancer[edit | edit source]

In esophageal cancer, DLEC1 is similarly inactivated through deletion or promoter hypermethylation. The re-expression of DLEC1 in esophageal cancer cells can suppress tumor growth, indicating its potential as a therapeutic target.

Clinical Implications[edit | edit source]

The frequent inactivation of DLEC1 in lung and esophageal cancers makes it a potential biomarker for diagnosis and prognosis. Additionally, therapies aimed at restoring DLEC1 function or expression could be beneficial in treating these cancers.

Research Directions[edit | edit source]

Ongoing research is focused on understanding the molecular mechanisms by which DLEC1 exerts its tumor suppressor effects. Studies are also exploring the potential of DLEC1 as a target for epigenetic therapy, aiming to reverse its silencing in cancer cells.

Conclusion[edit | edit source]

DLEC1 is a critical tumor suppressor gene involved in the pathogenesis of lung and esophageal cancers. Its frequent deletion or silencing in these cancers highlights its importance in maintaining normal cellular functions and preventing tumor development.


WikiMD
Navigation: Wellness - Encyclopedia - Health topics - Disease Index‏‎ - Drugs - World Directory - Gray's Anatomy - Keto diet - Recipes

Search WikiMD

Ad.Tired of being Overweight? Try W8MD's physician weight loss program.
Semaglutide (Ozempic / Wegovy and Tirzepatide (Mounjaro / Zepbound) available.
Advertise on WikiMD

WikiMD's Wellness Encyclopedia

Let Food Be Thy Medicine
Medicine Thy Food - Hippocrates

Medical Disclaimer: WikiMD is not a substitute for professional medical advice. The information on WikiMD is provided as an information resource only, may be incorrect, outdated or misleading, and is not to be used or relied on for any diagnostic or treatment purposes. Please consult your health care provider before making any healthcare decisions or for guidance about a specific medical condition. WikiMD expressly disclaims responsibility, and shall have no liability, for any damages, loss, injury, or liability whatsoever suffered as a result of your reliance on the information contained in this site. By visiting this site you agree to the foregoing terms and conditions, which may from time to time be changed or supplemented by WikiMD. If you do not agree to the foregoing terms and conditions, you should not enter or use this site. See full disclaimer.
Credits:Most images are courtesy of Wikimedia commons, and templates Wikipedia, licensed under CC BY SA or similar.

Contributors: Prab R. Tumpati, MD