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Collaboration Key to Cancer Findings

M. D. Anderson News Release 09/15/06

 When Baylor College of Medicine researcher Jun Qin, Ph.D., discovered a protein called MIP1 (or SIN1) in a proteomic analysis of a cellular pathway known to play a role in cancer development, he knew just the person he should seek as a collaborator - a colleague at The University of Texas M. D. Anderson Cancer Center.

That was the beginning of a partnership that resulted in a study appearing online in the journal Cell with both Qin, an associate professor in the BCM department of biochemistry and molecular biology, and Bing Su, Ph.D., M. D. Anderson professor of immunology, as senior authors.

Su and his colleagues had already made a mouse that lacked this protein (called a knockout), and suspected that MIP1 appeared in the critical mammalian TOR pathway that is a component of the PI3K/PTEN/Akt/TSC signaling pathway. When portions of either pathway are mutated, the cell takes a wrong turning and a variety of cancers can result.

Data from Qin's lab provided the first critical biochemical evidence for MIP1's role in this critical cellular pathway, Su said.

The pathway itself is activated through a process called phosphorylation in which two enzymes called kinases are involved. MIP1 is important because it is a critical protein in maintaining one of the complexes involved in this phosphorylation process.

Qin's laboratory does proteomics, the study of proteins and their functions. Proteins are the key components to cellular life and the proper operation of cells as they contribute to the life of an organism.

Su's laboratory contributed physiological and biological studies elucidating the pathway using his mouse that was bred to lack MIP1. Co-lead authors are Valeria Facchinetti, Ph.D., instructor of immunology at M. D. Anderson and Estela Jacinto, Ph.D., an assistant professor at the University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School in Piscataway, who is an expert in the yeast mTOR pathway.

"Dr. Jacinto understood the pathway well," said Qin.

Qin said that such collaborations are becoming more and more important. "Biological research requires such specialized expertise, it is hard for one laboratory to have it all," he said.

Anderson's Su agreed, calling the alliance "a natural collaboration" that brought diverse strengths to bear on a complex issue.

Before this study, research seemed to point against involvement of MIP1 in the mTOR/akt pathway," Su said. "Our study, using genetics, proteomics, molecular biology and biochemistry very thoroughly demonstrates its role as a regulator of akt activation."

The mTOR/akt is so fundamentally important to cell growth and survival and to organ development, Su noted, that these findings open new avenues for research in aging, stress, diabetes, and cardiovascular development as well as cancer.

Other who contributed to the work include Su's laboratory manager Dou Liu, who analyzed the early development of the knockout mice to establish the knockout cell lines, and Shiniu Wei and Qiaojia Huang, M.D., all of M. D. Anderson; Sung Yun Jung, Ph.D., of BCM and Nelyn Soto of UMDNJ-Robert Wood Johnson in New Jersey.

Funding for this study came from the National Institutes of Health, the Cancer Center Core Grant, the Nuclear Receptor Signalling Atlas grant and the American Heart Association.

© 2015 The University of Texas MD Anderson Cancer Center