Nalini Chandar, Ph.D.

Downers Grove, IL

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Regulation of osteoblast function and differentiation by tumor suppressor genes

Our laboratory investigates the role of several tumor suppressor genes in osteoblast differentiation and in the genesis of osteosarcomas. P53 is a well- known tumor suppressor gene that is inactivated in a number of different cancers. We have found p53 inactivation in osteosarcomas to be unique in that loss of expression prevails more often than other forms of functional inactivation. In our work, we have identified several differentiation-related genes that are directly regulated by p53. More recently we have studied p53 regulated microRNAs during osteoblast differentiation. We have established p53 to be an important processor of cellular information from various pathways to determine the choice between proliferation, differentiation, cell cycle arrest and apoptosis. Current evidence suggests that p53 function is essential in bone remodeling without which normal regulation of bone differentiation is set out of balance. Retinoblastoma (Rb) is another tumor suppressor gene implicated in osteosarcomagenesis. It is well known that pediatric patients with primary retinoblastoma tumors usually have secondary tumors in bone during their growth spurt. More recent evidence suggests that Rb might play a role in osteoblast differentiation from mesenchymal stem cells. Menin is another tumor suppressor gene that functions in pathways where Rb is involved. Both Rb and Menin have been implicated in the chromatin-mediated regulation of gene expression.


Research projects

Project I: Understand the role of specific microRNAs in mesenchymal and osteoblast differentiation. Our initial analyses of 3000 different microRNAs have identified several microRNAs that might play a role in osteoblast cell fate determination. We have extended these studies to specific microRNAs regulated by menin, p53 and Rb. This project will further analyze specific microRNAs and their roles in aiding menin, p53 and Rb mediated differentiation of the bone phenotype.

 Project II: Role of retinoblastoma in the regulation of osterix. Our preliminary data has identified osterix a bone specific transcription factor to be the target of retinoblastoma protein. This project will analyze the mechanism of action of retinoblastoma and its binding proteins in the regulation of osterix during osteoblast differentiation from stem cells. These studies will help identify mechanisms important for osteoblast differentiation from mesenchymal stem cells and aid in our understanding of why Rb function is critical for osteoblast fate determination.

 Project III:  Relationship between retinoblastoma and menin during osteoblast differentiation. Our preliminary studies and current evidence in the literature suggests that the relationship between the two tumor suppressors is important for cell fate determination and differentiation and is mediated through chromatin modifying proteins associated with Rb and Menin. These studies will attempt to dissect pathways and genes that are regulated by menin and Rb during stem cell differentiation. 


Downers Grove, IL

Chicago College of Osteopathic Medicine
College of Dental Medicine-Illinois

Biochemistry and Molecular Genetics

Dental Medicine
Osteopathic Medicine

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University of Madras | 1987 | Ph.D.
Andhra University | 1981 | M.S.

Courses Taught

Selected lectures and facilitation of Team-based workshops in:

Chicago College of Osteopathic Medicine (CCOM):

  • Biochemistry 1501: Human Clinical Biochemistry and Metabolism
  • Biochemistry 1502: Human Cell and Molecular Biology, Genetics and Nutrition - Course Director

Chicago College of Pharmacy (CCP):

  • Biochemistry 1555: Biochemistry II 

College of Dental Medicine - Illinois (CDMI)

Integrated Basic Science Sequence (IBSS):

  • IBSS 1520: Cell Function

College of Health Sciences (CHS):

  • Biochemistry 0551: Human Biochemistry (PA)
  • Biochemistry 0552: Clinical Biochemistry and Nutrition (PA)
  • Biochemistry 0520/0570: Biochemistry II (MABS/MBS)


Text Book  :  

 Chandar& Viselli- Cell and Molecular Biology ( Lippincott Illustrated Reviews Series (2018)

Chandar & Viselli- Cell and Molecular Biology (Lippincott Illustrated Reviews Series) (2010)


Selected Publications

Preclinical Evaluation of the Aurora Kinase inhibitors AMGi900, AZD1152-HQPA, and MK-5108 on SW872 and 93T449 human liposarcoma cells.
Norhoha S, Lauren AC Alt, Zarou O., Zanotti B., Mathur S., Rojas J., Chandar N., Fay MJ In Vitro Cell. Dev. Biol-Animal 2017   DOI: 10.1007/s11626-017-0208-4    PMID: 29197031  

In Vitro differentiation of preosteoblasts like cells MC3T3-E1 is enhanced by 1,25 dihydroxyvitamin D3. Pendleton, E & Chandar N
Frontiers Endocrinology 2017, PMID: 28670298

Gene expression profiles resulting from stable loss of p53 mirrors its role in tissue differentiation.  Couture O, Lombardi E, Davis K, Hays E, Chandar N.    PLoS One. 2013 Nov 28;8(11):e82494. doi: 10.1371/journal.pone.0082494. eCollection 2013.

Vitamin D directly regulates Mdm2 gene expression in osteoblasts. Chen H, Reed G, Guardia J, Lakhan S, Couture O, Hays E, Chandar N. Biochem Biophys Res Commun. 2013 Jan 4;430(1):370-4. doi: 10.1016/j.bbrc.2012.11.003. Epub 2012 Nov 10.

 Effects of cadmium on the sub-cellular localization of β-catenin and β-catenin-regulated gene expression in NRK-52E cells. Edwards JR, Kolman K, Lamar PC, Chandar N, Fay MJ, Prozialeck WC. Biometals. 2013 Feb;26(1):33-42. doi: 10.1007/s10534-012-9592-0. Epub 2012 Oct 19.

  p53 and MDM2 are involved in the regulation of osteocalcin gene expression. Chen H, Kolman K, Lanciloti N, Nerney M, Hays E, Robson C, Chandar N. Exp Cell Res. 2012 May 1;318(8):867-76. doi: 10.1016/j.yexcr.2012.02.022. Epub 2012 Mar 3. Erratum in: Exp Cell Res. 2012 Oct 1;318(16):2153.

 Osteocalcin gene expression is regulated by wild-type p53. Chen H, Hays E, Liboon J, Neely C, Kolman K, Chandar N. Calcif Tissue Int. 2011 Nov;89(5):411-8. doi: 10.1007/s00223-011-9533-x. Epub 2011 Oct 1.

 Beta-catenin is not activated by downregulation of PTEN in osteoblasts. Hays E, Schmidt J, Chandar N. In Vitro Cell Dev Biol Anim. 2009 Jul-Aug;45(7):361-70. doi: 10.1007/s11626-009-9189-2. Epub 2009 Apr 4.

 Effect of overexpression of estrogen receptors in osteoblasts. Harmston WR, Taddayon P, Kolman K, Chandar N. In Vitro Cell Dev Biol Anim. 2005 Sep-Oct;41(8-9):264-71.

 P53 and beta-catenin activity during estrogen treatment of osteoblasts. Chandar N, Saluja R, Lamar PC, Kolman K, Prozialeck WC. Cancer Cell Int. 2005 Jul 29;5:24.

 Relationship of bone morphogenetic protein expression during osteoblast differentiation to wild type p53. Chandar N, Swindle J, Szajkovics A, Kolman K. J Orthop Res. 2005 Nov;23(6):1345-53. Epub 2005 Jul 1.

 Gene expression changes accompanying p53 activity during estrogen treatment of osteoblasts. Chandar N, Logan D, Szajkovics A, Harmston W. Life Sci. 2004 Sep 10;75(17):2045-55.

 Induction of p53 expression and function by estrogen in osteoblasts. Bovenkerk S, Lanciloti N, Chandar N. Calcif Tissue Int. 2003 Sep;73(3):274-80.

 Reduction in p53 gene dosage diminishes differentiation capacity of osteoblasts. Chandar N, Donehower L, Lanciloti N.Anticancer Res. 2000 Jul-Aug;20(4):2553-9.

 p53 transactivity during in vitro osteoblast differentiation in a rat osteosarcoma cell line. Schwartz KA, Lanciloti NJ, Moore MK, Campione AL, Chandar N. Mol Carcinog. 1999 Jun;25(2):132-8.

 Hepatic hyperplasia and cancer in rats: metabolic alterations associated with cell growth. Rao KN, Elm MS, Kelly RH, Chandar N, Brady EP, Rao B, Shinozuka H, Eagon PK. Gastroenterology. 1997 Jul;113(1):238-48.

 Di(2-ethylhexyl)phthalate-induced changes in liver estrogen metabolism and hyperplasia. Eagon PK, Chandar N, Epley MJ, Elm MS, Brady EP, Rao KN. Int J Cancer. 1994 Sep 1;58(5):736-43.

 Dependence of induction of osteocalcin gene expression on the presence of wild-type p53 in a murine osteosarcoma cell line. Chandar N, Campbell P, Novak J, Smith M. Mol Carcinog. 1993;8(4):299-305.

 Low frequency of retinoblastoma gene alterations in rat hepatocellular carcinomas. Smith ML, Chandar N, Lombardi B.Mol Carcinog. 1993;8(4):228-33.

 Inactivation of p53 gene in human and murine osteosarcoma cells. Chandar N, Billig B, McMaster J, Novak J.Br J Cancer. 1992 Feb;65(2):208-14.

 Nutritional model of hepatocarcinogenesis. Rats fed choline-devoid diet. Lombardi B, Chandar N, Locker J. Dig Dis Sci. 1991 Jul;36(7):979-84. Review.

 Preneoplastic and neoplastic lesions in the pancreas of rats fed choline-devoid or choline-supplemented diets. Longnecker DS, Chandar N, Sheahan DG, Janosky JE, Lombardi B. Toxicol Pathol. 1991;19(1):59-65.

 Persistent reduction of indigenous DNA modification (I-compound) levels in liver DNA from male Fischer rats fed choline-devoid diet and in DNA of resulting neoplasms. Li DH, Xu DC, Chandar N, Lombardi B, Randerath K. Cancer Res. 1990 Dec 1;50(23):7577-80.

 No enhancement by phenobarbital of the hepatocarcinogenicity of a choline-devoid diet in the rat. Saito R, Chandar N, Janosky JE, Lombardi B. Res Commun Chem Pathol Pharmacol. 1990 Aug;69(2):197-207.

 c-myc gene amplification during hepatocarcinogenesis by a choline-devoid diet. Chandar N, Lombardi B, Locker J. Proc Natl Acad Sci U S A. 1989 Apr;86(8):2703-7.

 Reduced accumulation of I-compounds in liver DNA of rats fed a choline-devoid diet.  Li D, Chandar N, Lombardi B, Randerath K. Carcinogenesis. 1989 Mar;10(3):605-7.

 Liver cell proliferation and incidence of hepatocellular carcinomas in rats fed consecutively a choline-devoid and a choline-supplemented diet.  Chandar N, Lombardi B. Carcinogenesis. 1988 Feb;9(2):259-63.

 Analysis of ras genes and linked viral sequences in rat hepatocarcinogenesis. Chandar N,Lombardi B, Schulz W, Locker J. Am J Pathol. 1987 Nov;129(2):232-41.

 Liver cell turnover in rats fed a choline-devoid diet. Chandar N, Amenta J, Kandala JC, Lombardi B. Carcinogenesis. 1987 May;8(5):669-73.



Member- American Association for Cancer Research (1988- present)

Member- Women in Cancer Research (1995- present)

Member- AACR- Tumor Microenvironment Working Group 2006-present  

Member- Society for Invitro Biology

Member- The Association of Medical and Graduate Departments of Biochemistry     



2007-2012          NIH R15 AREA GRANT $209,995 (Total Costs)-  To study the role of p53 in differentiation 

2003- 2007         NIH R15 AREA GRANT $ 138,400 (Total costs)-To study role of p53 in bone differentiation

2002-2003          ILEX_ONCOLOGY: $ 36,000-  Apomine® and its analogues on osteoblast differentiation.

2001-2002            NIH Interim funding $ 10,000 (direct)    To continue work started on the first R15.              

1997-00               NIH R15 AREA Award (Total Costs $102,532)-  To study the role of p53 in bone differentiation



2018-present     Associate Editor BMC-Cancer (Springer Nature)

2016- present   Reviewer- AOA Research grants and abstracts

2002-2003        Reviewer: NIH Pathology B Study Section

2003-2007       Reviewer NIH Tumor Progression and Metastasis Study Section

2003                Reviewer: NIH Special Emphasis Panel Tumor Biology and Invasion