Joshua X. Gonzales

The University of Texas Southwestern Medical Center

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Melanie H. Cobb

The University of Texas Southwestern Medical Center

John D. Minna

The University of Texas Southwestern Medical Center

Elma Zaganjor

Vanderbilt University

Ashwinikumar Kulkarni

The University of Texas Southwestern Medical Center

Jill E. Larsen

University of Queensland

Ignacio I. Wistuba

The University of Texas MD Anderson Cancer Center

Jihan K. Osborne

The University of Texas Southwestern Medical Center

Mitsuo Sato

Nagoya University

Lauren M. Weil

The University of Texas Southwestern Medical Center

Misty Dawn Shields

Indiana University Health

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The University of Texas Southwestern Medical Center

Southwestern Medical Center

Harold C. Simmons Comprehensive Cancer Center

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The University of Texas MD Anderson Cancer Center

Harvard University

Harvard University Press

Center for Systems Biology

The University of Texas at Dallas

The University of Texas Health Science Center at San Antonio

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Ras transformation uncouples the kinesin-coordinated cellular nutrient response

Proceedings of the National Academy of Sciences (2014)

Elma Zaganjor Lauren M. Weil Joshua X. Gonzales John D. Minna Melanie H. Cobb

Significance The kinesin family member 2C (KIF2C) that regulates microtubule depolymerization, is up-regulated in a number of human cancer cells in a Ras- and ERK1/2-dependent manner. In this study, we find that KIF2C expression positively regulates signaling pathways downstream of Ras, ERK1/2, and mechanistic target of rapamycin complex 1 in nontransformed cells to coordinate a cellular nutrient response. Transformation by oncogenic Ras overrides the need for this level of organization and repurposes ERK1/2 and KIF2C signaling events. Therefore, this study provides a link for how cytoskeletal transformation may interconnect with cancer metabolism.

Kinesin

10.1073/pnas.1411016111

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NeuroD1 regulates survival and migration of neuroendocrine lung carcinomas via signaling molecules TrkB and NCAM

Proceedings of the National Academy of Sciences (2013)

Jihan K. Osborne Jill E. Larsen Misty Dawn Shields Joshua X. Gonzales David S. Shames

Small-cell lung cancer and other aggressive neuroendocrine cancers are often associated with early dissemination and frequent metastases. We demonstrate that neurogenic differentiation 1 (NeuroD1) is a regulatory hub securing cross talk among survival and migratory-inducing signaling pathways in neuroendocrine lung carcinomas. We find that NeuroD1 promotes tumor cell survival and metastasis in aggressive neuroendocrine lung tumors through regulation of the receptor tyrosine kinase tropomyosin-related kinase B (TrkB). Like TrkB, the prometastatic signaling molecule neural cell adhesion molecule (NCAM) is a downstream target of NeuroD1, whose impaired expression mirrors loss of NeuroD1. TrkB and NCAM may be therapeutic targets for aggressive neuroendocrine cancers that express NeuroD1.

Neuroendocrine differentiation

10.1073/pnas.1303932110

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Citations (94)