About

Professor Chendil Damodaran is associated with the Texas A&M Irma Lerma Rangel College of Pharmacy. The provided page text does not include specific details about his research focus, background, or key contributions. Therefore, a detailed professional biography cannot be extracted from the given information.

Research topics

• Biology
• Cancer research
• Cell biology
• Biochemistry
• Chemistry
• Computational biology
• Genetics
• Stereochemistry

Selected publications

• Arsenic exposure and prostate cancer risk: analysis of recent epidemiological evidence from Chile

  Annals of Cancer Epidemiology · 2026-04-01

  articleOpen accessSenior author
  PublisherDOI

• Therapeutic resistance and combination therapy for cancer: recent developments and future directions

  Scientific Reports · 2025-07-24 · 10 citations

  editorialOpen access1st author

  The diverse and heterogeneous nature of cancer is a fundamental characteristic that is responsible for therapy resistance, progression, and recurrence of disease. In order to enhance therapeutic efficacy, novel combination therapies are currently being proposed and utilized in clinical practice to effectively manage or retard disease progression. Several factors contribute to therapeutic resistance, including elevated expression of survival factors, mutations in genes that limit therapeutic effectiveness, multidrug resistance, and the potential involvement of cancer stem cells. This Scientific Reports Collection covers the underlying mechanisms responsible for therapeutic resistance. Additionally, the publications from this Collection highlight numerous innovative molecules to overcome this resistance and significantly sensitize tumors across various cancer models.

  PublisherOA PDFDOI

• Interaction between NF-κB and PLAC8 impairs autophagy providing a survival advantage to prostate cells transformed by cadmium

  Science Advances · 2025-06-13 · 4 citations

  articleOpen accessSenior authorCorresponding

  Prostate cancer risk is influenced by various factors, including exposure to heavy metals like cadmium (Cd). The study reveals that the autophagy-regulating gene PLAC8 (placenta-specific 8) is significantly involved in Cd-induced prostate carcinogenesis, and NF-κB acts as the upstream transcriptional activator of PLAC8, which then selectively up-regulates BCL-xL, providing a survival advantage to Cd-transformed cells. NF-κB activation stabilizes PLAC8 in the cytosol, disrupting autophagy by allowing PLAC8 to colocalize with LC3B instead of LAMP1. Silencing NF-κB down-regulates PLAC8 and its survival function while inhibiting NF-κB or PLAC8, which restores autophagy and decreases tumor growth in xenograft models. In addition, targeting BCL-xL confirmed this signaling pathway. The findings suggest that sustained NF-κB activation regulates PLAC8 and highlights the NF-κB-PLAC8-BCL-xL axis as a potential target for early detection and therapies in metal-induced prostate cancer.

  PublisherDOI

• Mechanistic role of metal-responsive transcription factor-1 (MTF-1) in cadmium-induced prostate carcinogenesis

  International Journal of Biological Sciences · 2025-05-27 · 3 citations

  articleOpen accessSenior author

  Our previous report emphasized that chronic exposure to cadmium (10 µM) over one year led to the transformation of benign prostatic hyperplasia (BPH1) cells into malignancy through the ZIC2 signaling pathway (cerebellar zinc pathway). However, the upstream mechanisms that trigger this transformation have yet to be fully elucidated. The present study suggests that cadmium exposure induces metal regulatory element-binding transcription factor-1 (MTF1), which activates ZIC2 in BPH1 cells. Interestingly, knocking out ZIC2 expression did not affect MTF1 levels, indicating that MTF1 acts upstream of the ZIC2 signaling pathway. To further investigate the MTF-1/ZIC2 relationship, we overexpressed MTF-1 in untransformed BPH1 cells leading to the induction of ZIC2 along with other stem cell markers, such as ALDH1A1, Nanog, and CD44. This overexpression also facilitated spheroid formation. Conversely, silencing MTF1 expression in transformed cells inhibited spheroid formation and also reduced survival rate. It diminished the expression of stem cell and epithelial-to-mesenchymal transition markers and tumor growth in nude mice. Transcriptomic analysis of MTF1 silenced xenograft tumors confirmed these findings. Using CRISPR-Cas9 to knock out ZIC2 also prevented tumor formation in nude mice. These results emphasize the critical role of MTF1 in the oncogenic process and its involvement in the ZIC2-mediated transformation associated with Cd-induced malignant changes.

  PublisherOA PDFDOI

• INGESTION OF INORGANIC ARSENIC IN DRINKING WATER INDUCED UROGENITAL CARCINOGENESIS IN MICE MODELS

  Urologic Oncology Seminars and Original Investigations · 2024-03-01 · 1 citations

  articleSenior author
  PublisherDOI

• Scientific methods

  Elsevier eBooks · 2024-10-04

  book-chapterSenior author
  PublisherDOI

• Abstract 7198: A small molecule Notch1 inhibitor (ASR490) restores chemosensitivity in triple-negative breast cancer

  Cancer Research · 2024-03-22

  articleSenior author

  Abstract Metastatic triple-negative Breast cancer (mTNBC) is an aggressive and often a chemo resistant disease for which no effective druggable target has yet been identified. We and others reported that the aberrant expression of neurogenic locus Notch homolog protein 1 (Notch1) serves as a molecular signature for TNBC. Hence, we postulated that pharmacologically targeting Notch1 in conjunction with a standard chemotherapeutic agent (Doxorubicin: DXR) may completely eradicate TNBC growth and overcome systemic and debilitating toxicity. Hence, this study aims to elucidate the role of our recently discovered notch1 inhibitor ASR490 and its ability to chemosensitize TNBC without significant systemic toxicity. In our results, pretreatment of 1/10 th of the inhibitory concentration of ASR490 combined with 1/10 th or 1/20th of DXR significantly inhibited the growth of TNBC cells (MDA-MB-231 and BT549). Notably, DXR treatment induced Notch1 activation which led to chemoresistance in TNBC; however, co-treatment with the Notch1 inhibitor ASR490, led to the downregulation of Notch1 activation and eradication of the cell viability and clonogenicity of the TNBC cells. Further, molecular analysis suggested that pretreatment of 1/10th of ASR490 facilitates DXR-mediated sensitivity, by inhibiting the DNA repair pathway and upregulating (cleaved) caspase 3, (cleaved) caspase-9 and poly (ADP-Ribose) polymerase (PARP)-mediated apoptosis. Similarly, the combination effectively blocked the epithelial and mesenchymal transition (EMT) regulators and suppressed metastatic properties of MDA-MB231 and BT-549 cells. Moreover, combining ASR490(1/10th) and DXR (1/20th) significantly eradicated xenotransplanted TNBC tumors compared to ASR490 or DXR alone. In addition to being effective at inhibiting tumor growth, the significantly lower dose requirements of DXR and ASR490 in combination makes it a highly safe therapeutic modality. These findings suggest that aberrant activation of Notch1 is responsible for TNBC chemoresistance and concomitantly inhibiting Notch1 activation is an effective therapeutic strategy to restore chemosensitivity in TNBC. Citation Format: Neha Tyagi, Balaji Chandrasekaran, Ashish Tyagi, Balpreet Singh, Megha Chandran, Amandeep Singh, Arun Sharma, Chendil Damodaran. A small molecule Notch1 inhibitor (ASR490) restores chemosensitivity in triple-negative breast cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 7198.

  PublisherDOI

• Corrigendum: A small molecule inhibitor of Notch1 modulates stemness and suppresses breast cancer cell growth

  Frontiers in Pharmacology · 2024-05-27 · 1 citations

  erratumOpen accessSenior authorCorresponding

  [This corrects the article DOI: 10.3389/fphar.2023.1150774.].

  PublisherOA PDFDOI

• Abstract 1473: Exposure of arsenic promotes malignant stemness and induces bladder malignancy in preclinical models

  Cancer Research · 2024-03-22

  articleSenior author

  Abstract Numerous epidemiological and scientific studies have consistently demonstrated that populations exposed to arsenic (As) concentrations ranging from >10 ppb to 2500 ppb in their drinking water face an elevated risk of urogenital cancers, with a particular emphasis on bladder cancer (BCa). Hence, the goal of the study is to investigate the underlying mechanisms that trigger malignant transformation in the bladder using physiologically relevant arsenic concentrations observed in BCa patients. In our results, we observed significantly elevated levels of arsenic in the urine of BCa patients, ranging from 20 to 50 mg/L, in stark contrast to the levels observed in healthy controls (>10 mg/L) and the recommended guidelines set by the Environmental Protection Agency (EPA) and Centers for Disease Control and Prevention (CDC). We used a median physiological concentration of arsenic (30 PPM) in drinking water-induced bladder hyperplasia in male and female mice over six months. Likewise, chronic exposure of healthy bladder epithelial cells (TRT-HU1) to similar arsenic concentrations (250nM:30 PPM) for 12 months resulted in malignant transformation, and arsenic-transformed cells (AsT) were capable of inducing tumors in xenografted and orthotopic models. Nonetheless, the molecular mechanism responsible for this malignancy remains to be elucidated. Our molecular analysis has pointed towards the activation of stem cells, notably ALDH1A1 (with a 50,000-fold increase), as a pivotal factor driving this transformation. Furthermore, our research has demonstrated that the activation of ALDH1A1 is contingent on the induction of Metal Response Element-Binding Transcription Factor-1 (MTF1). Consequently, silencing MTF1 inhibited the expression of ALDH1A1 and its associated malignant properties in As-transformed cells, strongly suggesting that MTF1 functions as the master regulator in As-induced bladder carcinogenesis. We have also observed similar molecular signatures (MTF1 and ALDH1A1 expression) in arsenic-exposed versus non-exposed mice and bladder cancer patients. In conclusion, our studies suggest that activation of stem cells is a critical step in arsenic-induced bladder carcinogenesis. Citation Format: Bhawna Tyagi, Mohit Vashishta, Neha Tyagi, Balaji Chandrasekaran, Vaibhav Shukla, Ashish Tyagi, Chendil Damodaran. Exposure of arsenic promotes malignant stemness and induces bladder malignancy in preclinical models [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 1473.

  PublisherDOI

• List of contributors

  Elsevier eBooks · 2024-10-04

  book-chapterOpen access
  PublisherDOI

Recent grants

• Targeting AR and Akt for the Treatment of Prostate Cancer

  NIH · $1.5M · 2014–2018

• Cell Survival Advantage in Cadmium Induced Carcinogenesis

  NIH · $2.3M · 2021–2026

• The role of autophagy in cadmium induced prostate carcinogenesis

  NIH · $1.9M · 2021–2024

• Chemoprevention of metastatic colorectal cancer

  NIH · $2.0M · 2014–2020

• NIH Grant R21CA143456

  NIH · $318k · 2013

Frequent coauthors

• Trinath P. Das

  University of Chicago

  66 shared

• Murali K. Ankem

  64 shared

• Suman Suman

  59 shared

• Ashish Tyagi

  52 shared

• Balaji Chandrasekaran

  Saveetha University

  51 shared

• Sowmyalakshmi Srinivasan

  39 shared

• Venkatesh Kolluru

  University of Louisville

  35 shared

• Arun Sharma

  Pennsylvania State University

  29 shared

Labs

• Pharmaceutical SciencesPI

Education

• PhD, Urology

  University of louisville

  2021

Awards & honors

• Presidential Impact Fellow