About

Carisa Armstrong is an Associate Professor at Texas A&M University College of Performance, Visualization & Fine Arts. Her scholarly interests include Dance Science, Pilates Training, and Choreography. She holds a Master of Fine Arts in Dance from Case Western Reserve University, Cleveland, Ohio, earned in 2002 with an emphasis in pedagogy, performance, and choreography. Additionally, she earned a Bachelor of Exercise and Sports Science from Southwest Texas State University in San Marcos, Texas, in 1999, with an emphasis in Dance and Secondary Education. Her educational background and professional focus reflect a dedication to the integration of dance, performance, and health sciences.

Research topics

• Medicine
• Cancer research
• Biology
• Internal medicine
• Pathology
• Endocrinology
• Genetics
• Oncology
• Pharmacology
• Cell biology
• Biochemistry

Selected publications

• Steroid Sulfatase Regulates Metabolic Reprogramming in Advanced Prostate Cancer

  Cancers · 2025-06-12 · 1 citations

  articleOpen access

  BACKGROUND/OBJECTIVE: The expression of human steroid sulfatase (STS) is upregulated in castration-resistant prostate cancer (CRPC) and is associated with resistance to anti-androgen drugs, such as enzalutamide (Enza) and abiraterone (Abi). Despite the known link between STS overexpression and therapeutic unresponsiveness, the mechanism by which STS confers this phenotype remains incompletely understood. In this study, we sought to understand how STS induces treatment resistance in advanced prostate cancer (PCa) cells by exploring its role in altering mitochondrial activity. METHODS: To examine the effects of increased STS expression on mitochondrial respiration and programming, we performed RNA sequencing (RNA-seq) analysis, the Seahorse XF Mito Stress Test, and a mitochondrial Complex I enzyme activity assay in STS-overexpressing cells (C4-2B STS) and in enzalutamide-resistant CPRC cells (C4-2B MDVR). We employed SI-2, the specific chemical inhibitor of STS, on C4-2B STS and C4-2B MDVR cells and evaluated STS activity inhibition on mitochondrial molecular pathways and mitochondrial respiration. Lastly, we examined the effects of dehydroepiandrosterone sulfate (DHEAS) supplementation on C4-2B STS organoids. RESULTS: We present evidence from the transcriptomic profiling of C4-2B STS cells that there are enriched metabolic pathway signatures involved in oxidative phosphorylation, the electron transport chain, and mitochondrial organization. Moreover, upon STS inhibition, signaling in the electron transport chain and mitochondrial organization pathways is markedly attenuated. Findings from the Seahorse XF Mito Stress Test and mitochondrial Complex I enzyme activity assay demonstrate that STS overexpression increases mitochondrial respiration, whereas the inhibition of STS by SI-2 significantly reduces the oxygen consumption rate (OCR) and Complex I enzyme activity in C4-2B STS cells. Similarly, an increased OCR and electron transport chain Complex I enzymatic activity are observed in C4-2B MDVR cells and a decreased OCR upon SI-2 inhibition. Lastly, we show that STS overexpression promotes organoid growth upon DHEAS treatment. CONCLUSIONS: Our study demonstrates STS as a key driver of metabolic reprogramming and flexibility in advanced prostate cancer. Disrupting enhanced mitochondrial respiration via STS presents a promising strategy in improving CRPC treatment.

  PublisherOA PDFDOI

• Synthesis of Solid-Solution Mn_<i>x</i>Zn_1–<i>x</i>O Nanoparticles and their Electrochemical Oxidation of Furfural

  Inorganic Chemistry · 2025-08-20

  article

  Electrochemical valorization of biomass-derived substrates has become a prominent area of research due to its potential to produce value-added products from renewable feedstocks in a more sustainable way. First-row transition-metal electrodes are compelling candidates for these conversions due to their stability, abundance, and cost-effectiveness. Herein, we report on the colloidal synthesis of MnxZn1–xO (x = 0.3–0.7) nanoparticles and their electrocatalytic activity toward furfural oxidation. We find that the hindrance of a MnO impurity can be achieved by leveraging the oxidation state of the Mn precursor. The MnxZn1–xO composition closely follows the ratio of precursors, with all of the nanoparticles having a wurtzite structure as determined by ICP-MS and PXRD, respectively. XANES and XPS revealed the presence of Mn in different oxidation states, with the ratio of these varying based on the composition. When comparing the electrocatalytic activity of the monometallic and bimetallic oxides for furfural oxidation, a decrease in current density was observed with increasing Zn content. We find that the MnxZn1–xO nanoparticles favor the formation of the 6 e– oxidation product 5-hydroxy-2(5H)-furanone, while both monometallic oxides primarily yield CO2 and other deeply oxidized products. These findings can contribute toward the design and synthesis of more active and selective electrocatalysts.

  PublisherDOI

• Novel dual inhibitors of AR/AR variants and AKR1C3: Preclinical activities for advanced prostate cancer therapy.

  Journal of Clinical Oncology · 2024-01-29

  article

  169 Background: AR/AR-variants and AKR1C3 play critical roles in prostate cancer progression and driving resistance to antiandrogens, and are attractive targets for therapeutic intervention for advanced prostate cancer. However, there are currently no clinically available therapies that simultaneously target both AR/AR variants and AKR1C3. We have developed the novel small molecule inhibitors, LX-1 and its analog LX-1S, which target both the AR-V7 splice variant and the enzyme AKR1C3. Methods: A library of the LX compounds was designed and synthesized according to structure based computer modeling. The effects of the lead LXs on the expression and activity of AR/AR-variants and AKR1C3 were evaluated. RNA-seq was performed on the lead LXs. Resistant cell sublines generated from C4-2B cells resistant to enzalutamide (MDVR), apalutamide (ApalR), darolutamide (DaroR), or abiraterone (AbiR) were treated with LX-1 or their respective antiandrogen. Mice bearing VCaP xenograft tumors and LuCaP35CR PDX tumors were treated with LX-1/LX-1s and effects on tumor growth were assessed. Results: Molecular docking studies and in vitro experiments demonstrated that LX compounds effectively bind to the AKR1C3 active site and inhibit AKR1C3 enzymatic activity. LX compounds were also shown to reduce AR/AR-V7 expression and inhibit their target gene signaling, induce G0/G1 arrest in anti-androgen resistant cell lines. LX-1/LX-1S treatment resulted in reduced tumor volumes and decreased intratumoral testosterone in both xenograft tumor and PDX models. LX-1 effectively inhibited the conversion of androstenedione into testosterone in tumor-based ex vivo enzyme assays. Moreover, LX-1 synergized with enzalutamide and abiraterone as well as docetaxel, suggesting its potential to enhance the anti-tumor activity of these standard therapies in resistant prostate cancer. Furthermore, LX-1/LX-1S improved enzalutamide treatment in resistant prostate cancer tumor models. Notably, LX-1S demonstrates significantly better bioavailability and efficacy than LX-1 in reducing resistant cell growth in both in vitro and in vivo animal models. Conclusions: Our study unveils the potential of LX compounds, especially LX-1 and its analog LX-1S, as promising therapeutic agents for advanced prostate cancer. These compounds not only inhibit AR and AKR1C3 signaling but also suppress resistant tumor growth and synergize with antiandrogens to enhance their therapeutic efficacy.

  PublisherDOI

• Correction: Niclosamide enhances abiraterone treatment via inhibition of androgen receptor variants in castration resistant prostate cancer

  Oncotarget · 2024-01-06

  erratumOpen access
  PublisherDOI

• Data from LX1 Dual Targets AR Variants and AKR1C3 in Advanced Prostate Cancer Therapy

  2024-11-04

  preprintOpen access

  &lt;div&gt;Abstract&lt;p&gt;The development of resistance to current standard-of-care treatments, such as androgen receptor (AR) targeting therapies, remains a major challenge in the management of advanced prostate cancer. There is an urgent need for new therapeutic strategies targeting key resistant drivers, such as AR variants like AR-V7, and steroidogenic enzymes, such as aldo–keto reductase 1C3 (AKR1C3), to overcome drug resistance and improve outcomes for patients with advanced prostate cancer. Here, we have designed, synthesized, and characterized a novel class of LX compounds targeting both the AR/AR variants and AKR1C3 pathways. Molecular docking and &lt;i&gt;in vitro&lt;/i&gt; studies demonstrated that LX compounds bind to the AKR1C3 active sites and inhibit AKR1C3 enzymatic activity. LX compounds were also shown to reduce AR/AR-V7 expression and to inhibit their target gene signaling. LX1 inhibited the conversion of androstenedione into testosterone in tumor-based &lt;i&gt;ex vivo&lt;/i&gt; enzyme assays. In addition, LX1 inhibited the growth of cells resistant to antiandrogens including enzalutamide (Enza), abiraterone, apalutamide, and darolutamide &lt;i&gt;in vitro&lt;/i&gt;. A synergistic effect was observed when LX1 was combined with antiandrogens and taxanes, indicating the potential for this combination in treating resistant prostate cancer. Treatment with LX1 significantly decreased tumor volume, serum PSA levels, as well as reduced intratumoral testosterone levels, without affecting mouse body weight. Furthermore, LX1 was found to overcome resistance to Enza treatment, and its combination with Enza further suppressed tumor growth in both the CWR22Rv1 xenograft and LuCaP35CR patient-derived xenograft models. Collectively, the dual effect of LX1 in reducing AR signaling and intratumoral testosterone, along with its synergy with standard therapies in resistant models, underscores its potential as a valuable treatment option for advanced prostate cancer.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Significance:&lt;/b&gt; LX1 simultaneously targets androgen receptor variants and the steroidogenic enzyme AKR1C3, offering a promising approach to combat drug resistance and enhancing therapeutic efficacy in conjunction with standard treatments for advanced prostate cancer.&lt;/p&gt;&lt;/div&gt;

  PublisherDOI

• LX1 Dual Targets AR Variants and AKR1C3 in Advanced Prostate Cancer Therapy

  Cancer Research · 2024-08-01 · 10 citations

  articleOpen access

  The development of resistance to current standard-of-care treatments, such as androgen receptor (AR) targeting therapies, remains a major challenge in the management of advanced prostate cancer. There is an urgent need for new therapeutic strategies targeting key resistant drivers, such as AR variants like AR-V7, and steroidogenic enzymes, such as aldo-keto reductase 1C3 (AKR1C3), to overcome drug resistance and improve outcomes for patients with advanced prostate cancer. Here, we have designed, synthesized, and characterized a novel class of LX compounds targeting both the AR/AR variants and AKR1C3 pathways. Molecular docking and in vitro studies demonstrated that LX compounds bind to the AKR1C3 active sites and inhibit AKR1C3 enzymatic activity. LX compounds were also shown to reduce AR/AR-V7 expression and to inhibit their target gene signaling. LX1 inhibited the conversion of androstenedione into testosterone in tumor-based ex vivo enzyme assays. In addition, LX1 inhibited the growth of cells resistant to antiandrogens including enzalutamide (Enza), abiraterone, apalutamide, and darolutamide in vitro. A synergistic effect was observed when LX1 was combined with antiandrogens and taxanes, indicating the potential for this combination in treating resistant prostate cancer. Treatment with LX1 significantly decreased tumor volume, serum PSA levels, as well as reduced intratumoral testosterone levels, without affecting mouse body weight. Furthermore, LX1 was found to overcome resistance to Enza treatment, and its combination with Enza further suppressed tumor growth in both the CWR22Rv1 xenograft and LuCaP35CR patient-derived xenograft models. Collectively, the dual effect of LX1 in reducing AR signaling and intratumoral testosterone, along with its synergy with standard therapies in resistant models, underscores its potential as a valuable treatment option for advanced prostate cancer. Significance: LX1 simultaneously targets androgen receptor variants and the steroidogenic enzyme AKR1C3, offering a promising approach to combat drug resistance and enhancing therapeutic efficacy in conjunction with standard treatments for advanced prostate cancer.

  PublisherOA PDFDOI

• An application of clustering to classify movement patterns in men’s professional grand slam hard court tennis

  International Journal of Performance Analysis in Sport · 2024-07-31 · 3 citations

  articleOpen access1st authorCorresponding

  The movement cycles from Australian Open player tracking data were analysed using the Lloyd k-means clustering algorithm to classify movement patterns that exist in men’s grand-slam tennis. The elbow criterion method identified six movement patterns, and the k-means model allocated each movement cycle into one of these discrete groups. A description of each movement pattern is presented, outlining three inner range and three end range movement patterns, which are distinguishable by distance, direction, time pressure, and starting location. These findings provide objective details for coaches and athletes to understand tennis movement, overcoming vague descriptions of the inner range and end range in tennis vernacular. The amalgam of distance, direction, and time pressure demands that categorise the six movement patterns can enhance the specificity of training drill design and movement evaluation. Furthermore, evaluating the movement patterns a player typically elicits during match-play can inform typical load exposure and be useful in load monitoring practices. Additionally, understanding the prevalence of movement patterns in a typical match may help understand the strategic approaches players use during match-play.

  PublisherOA PDFDOI

• Supplementary Information from LX1 Dual Targets AR Variants and AKR1C3 in Advanced Prostate Cancer Therapy

  2024-11-04

  preprintOpen access

  &lt;p&gt;Suppl. Figure 1-10, Table 1-2.&lt;/p&gt;

  PublisherDOI

• Unraveling the molecular and growth mechanism of colloidal black In₂O_3−<i>x</i>

  Nanoscale · 2024-01-01 · 3 citations

  articleOpen access1st author

  Precursors, ligands, and reaction environment dictate the path for the colloidal synthesis of oxygen-deficient black indium oxide nanoparticles with enhanced optical properties.

  PublisherOA PDFDOI

• IGFBP3 promotes resistance to Olaparib via modulating EGFR signaling in advanced prostate cancer

  iScience · 2024-01-19 · 11 citations

  articleOpen access

  Olaparib is a pioneering PARP inhibitor (PARPi) approved for treating castration-resistant prostate cancer (CRPC) tumors harboring DNA repair defects, but clinical resistance has been documented. To study acquired resistance, we developed Olaparib-resistant (OlapR) cell lines through chronic Olaparib treatment of LNCaP and C4-2B cell lines. Here, we found that IGFBP3 is highly expressed in acquired (OlapR) and intrinsic (Rv1) models of Olaparib resistance. We show that IGFBP3 expression promotes Olaparib resistance by enhancing DNA repair capacity through activation of EGFR and DNA-PKcs. IGFBP3 depletion enhances efficacy of Olaparib by promoting DNA damage accumulation and subsequently, cell death in resistant models. Mechanistically, we show that silencing IGFBP3 or EGFR expression reduces cell viability and resensitizes OlapR cells to Olaparib treatment. Inhibition of EGFR by Gefitinib suppressed growth of OlapR cells and improved Olaparib sensitivity, thereby phenocopying IGFBP3 inhibition. Collectively, our results highlight IGFBP3 and EGFR as critical mediators of Olaparib resistance.

  PublisherOA PDFDOI

Frequent coauthors

• Allen C. Gao

  VA Northern California Health Care System

  88 shared

• Wei Lou

  50 shared

• Christopher P. Evans

  UC Davis Comprehensive Cancer Center

  47 shared

• Chengfei Liu

  University of California, Davis

  41 shared

• Alan P. Lombard

  40 shared

• Joy C. Yang

  University of California, Davis

  24 shared

• Jinge Zhao

  Ministry of Industry and Information Technology

  21 shared

• Leandro S. D’Abronzo

  University of California, Davis

  20 shared

Labs

• Learning Interactive Visualization Experience Lab (LIVE Lab)PI