A biotherapy strategy for esophageal cancer in the future

April 19, 2010

A research team from China focused on esophageal squamous cell carcinoma (ESCC) and characterized sphingosine 1-phosphate (S1P) receptor expression pattern and investigated the role of S1P receptors on ESCC cells proliferation and migration. Their results showed that ESCC cells may down-regulate the expression of S1P5 to promote proliferation and escape S1P-S1P5 induced migration inhibition.

Esophageal cancer is one of the most common malignancies worldwide. Its mortality is very high due to relatively late diagnosis and inefficient treatment. The ability to reverse the outcome of esophageal cancer is limited due to a poor understanding of its biology. Progression of esophageal cancer may be associated with sphingosine 1-phosphate (S1P) and its S1P1-5, which play an important role in other cancers. A possible role for S1P and its receptors in human esophageal cells has not previously been investigated, nor has the importance of S1P and its receptors in esophageal cancer growth and metastasis been addressed.

Using semi-quantitative reverse transcription polymerase chain reaction, gene transfection, MTT assay and transwell migration assay, a research team from China investigated S1P receptor expression profile in human esophageal and the effects of S1P5 on proliferation and migration. Their study will be published on April 21, 2010 in the .

They found S1P binding to S1P5 inhibits the proliferation and migration of S1P5-transfected Eca109 cells.

Their results indicated that deficiency in inhibitory effect of S1P-S1P5 may be of importance in the growth and metastasis of esophageal cancer. S1P5 or its associated signaling molecules may serve as a future strategy in biotherapy for .

More information: Hu WM, Li L, Jing BQ, Zhao YS, Wang CL, Feng L, Xie YE. Effect of S1P5 on proliferation and migration of human esophageal cancer cells. World J Gastroenterol 2010; 16(15):1859-1866. www.wjgnet.com/1007-9327/full/v16/i15/1859.htm

Related Stories

Recommended for you

Study prompts new ideas on cancers' origins

December 16, 2017
Rapidly dividing, yet aberrant stem cells are a major source of cancer. But a new study suggests that mature cells also play a key role in initiating cancer—a finding that could upend the way scientists think about the ...

What does hair loss have to teach us about cancer metastasis?

December 15, 2017
Understanding how cancer cells are able to metastasize—migrate from the primary tumor to distant sites in the body—and developing therapies to inhibit this process are the focus of many laboratories around the country. ...

Cancer immunotherapy may work better in patients with specific genes

December 15, 2017
Cancer cells arise when DNA is mutated, and these cells should be recognized as "foreign" by the immune system. However, cancer cells have found ways to evade detection by the immune system.

Scientists pinpoint gene to blame for poorer survival rate in early-onset breast cancer patients

December 15, 2017
A new study led by scientists at the University of Southampton has found that inherited variation in a particular gene may be to blame for the lower survival rate of patients diagnosed with early-onset breast cancer.

Scientists unlock structure of mTOR, a key cancer cell signaling protein

December 14, 2017
Researchers in the Sloan Kettering Institute have solved the structure of an important signaling molecule in cancer cells. They used a new technology called cryo-EM to visualize the structure in three dimensions. The detailed ...

'Bet hedging' explains the efficacy of many combination cancer therapies

December 14, 2017
The efficacy of many FDA-approved cancer drug combinations is not due to synergistic interactions between drugs, but rather to a form of "bet hedging," according to a new study published by Harvard Medical School researchers ...

0 comments

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.