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Dr. Michelle A. Lane

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Dr. Michelle Lane

Associate Professor
PhD: Rutgers University, Nutritional Sciences
Phone: (512)245-4654
Office: FCS 281


Research Interests

I am the lead investigator on the Food Feelings and Family research study. Our goal is to determine how what a woman eats during pregnancy affects her risk for post-partum depression. For more information on our study, including how to participate, click here.

Research in my laboratory has two foci. The first concerns the ability of nutrients such as vitamin A and omega-3 fatty acids to prevent colon cancer metastasis. The second area, relates to the effect of diet on maternal and offspring behavior and brain metabolism. We use cellular models, rodent, and human subjects as well as biochemical and molecular techniques, spanning the molecular to population level, in our research.

We are currently determining how omega-3 fatty acids decrease colon cancer cell division and prevent metastasis using a variety of in vitro molecular techniques. We hope to expand this work and develop a clinically-relevant mouse model for colon cancer metastasis. Most mouse models for studying metastasis are immunodeficient and inject cells at sites unrelated to where the tumor originates in humans. For example, tumor cells would be injected subcutaneously or intrasplenically to study colon cancer metastasis. To overcome these shortcomings, we are currently developing a syngeneic, orthotopic mouse model to study the effect of diet on the immune system and colon cancer metastasis at the appropriate physiological site. The cells injected into the mice express luciferase, allowing us to detect the tumor cells in living mice and follow the metastatic progression.

Previously we have shown that omega-3 fatty acid supplementation increases the ability of rat mothers to adapt to stress.  Brains from dams were mapped for cytochrome oxidase (CO) activity with a quantitative histochemical method used to identify networks of altered brain regions. Omega-3 fatty acid supplementation appeared to increase white matter, consistent with the literature showing that omega-3 fatty acids promote myelination. We further identified a multiregional pattern of CO activity discriminating omega-3 fatty acid -deficient brains from omega-3 fatty acid -supplemented brains. These findings suggest that omega-3 fatty acid deficiency causes widespread disruption in the communication between brain regions, potentially mediated by decreased myelination. We are currently working to determine if myelination is affected and how.


Selected Publications

(for a complete bibliography, please see

  • Jackson C, Barrett DW, Shumake J, Gonzales E, Gonzalez-Lima F, Lane MA. Maternal omega-3 fatty acid intake during neurodevelopment does not affect pup behavior related to depression, novelty, or learning. BMC Res Notes. 2018 15;11(1):812. doi: 10.1186/s13104-0183915-3.

  • Applegate, Lane MA. Role of retinoids in the prevention and treatment of colorectal cancer. World J Gastrointest Oncol. 2015;7(10):184-203. doi: 10.4251/wjgo.v7.i10.184.

  • Gonzales E, Barrett DW, Shumake J, Gonzalez-Lima F, Lane MA. Omega-3 fatty acids improve behavioral coping to stress in multiparous rats. Behavioural brain research. 2015;279:129-38. Epub 2014/12/03. doi: 10.1016/j.bbr.2014.11.010. PubMed PMID: 25446767.

  • Shumake J, Barrett DW, Lane MA, Wittke AJ. Behavioral effects of bovine lactoferrin administration during postnatal development of rats. Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine. 2014;27(5):1039-55. Epub 2014/04/23. doi: 10.1007/s10534-014-9735-6. PubMed PMID: 24752859

  • Lengyel JN, Park EY, Brunson AR, Pinali D, Lane MA. Phosphatidylinositol 3-kinase mediates the ability of retinol to decrease colorectal cancer cell invasion. Nutrition and Cancer. 2014;66(8):1352-61. Epub 2014/10/31. doi: 10.1080/01635581.2014.956258. PubMed PMID: 25356626.

  • Park EY, Pinali D, Lindley K, Lane MA. Hepatic vitamin A preloading reduces colorectal cancer metastatic multiplicity in a mouse xenograft model. Nutrition and Cancer. 2012;64(5):732-40. Epub 2012/05/31. doi: 10.1080/01635581.2012.687425. PubMed PMID: 22642873; PMCID: PMC3829719.

  • Drew CJ, O'Reilly KC, Lane MA, Bailey SJ. Chronic administration of 13-cis-retinoic acid does not alter the number of serotoninergic neurons in the mouse raphe nuclei. Neuroscience. 2011;172:66-73. Epub 2010/10/28. doi: 10.1016/j.neuroscience.2010.10.050. PubMed PMID: 20977931; PMCID: PMC3386639.

  • O'Reilly KC, Shumake J, Bailey SJ, Gonzalez-Lima F, Lane MA. Chronic 13-cis-retinoic acid administration disrupts network interactions between the raphe nuclei and the hippocampal system in young adult mice. European Journal of Pharmacology. 2009;605(1-3):68-77. Epub 2009/01/27. doi: 10.1016/j.ejphar.2008.12.037. PubMed PMID: 19168052.

  • Park EY, Wilder ET, Chipuk JE, Lane MA. Retinol decreases phosphatidylinositol 3-kinase activity in colon cancer cells. Molecular Carcinogenesis. 2008;47(4):264-74. Epub 2007/10/06. doi: 10.1002/mc.20381. PubMed PMID: 17918208.

  • O'Reilly KC, Shumake J, Gonzalez-Lima F, Lane MA*, Bailey SJ*. Chronic administration of 13-cis-retinoic acid increases depression-related behavior in mice. Neuropsychopharmacology. 2006;31(9):1919-27. Epub 2006/01/06. doi: 10.1038/sj.npp.1300998. PubMed PMID: 16395305. *These authors contributed equally to this work.

  • Park EY, Dillard A, Williams EA, Wilder ET, Pepper MR, Lane MA. Retinol inhibits the growth of all-trans-retinoic acid-sensitive and all-trans-retinoic acid-resistant colon cancer cells through a retinoic acid receptor-independent mechanism. Cancer Research. 2005;65(21):9923-33. Epub 2005/11/04. doi: 10.1158/0008-5472.can-05-1604. PubMed PMID: 16267017.

Current Lab Members:

Graduate Students:

Crystal Alvarez
Rebecca Smith

Undergraduate Students:

John Muraida


Courses Currently Teaching:

Undergraduate Courses:

NUTR 4361, Biochemical Nutrition

NUTR 4362, Nutrition and Genetics


Graduate Courses:

NUTR 5367, Nutrient Metabolism II


Contact Information

Office - FCS 279
Phone: 512-245-4654
Office Hours: