About

Weston Porter is associated with the Texas A&M College of Veterinary Medicine & Biomedical Sciences (VMBS), which is ranked as the No. 3 veterinary college in the United States and No. 4 in the world for research in animal science and veterinary medicine. The college emphasizes a 'One Health' approach, recognizing the complex interactions between animal, human, and environmental health, and engages in cutting-edge basic and clinical research to address pressing scientific questions. The college supports collaborations that translate discoveries into proactive solutions for animal, human, and environmental health, and is involved in various educational, research, and outreach activities.

Research topics

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

Selected publications

• Detecting supramolecular organic nanoparticles during heat wave

  Science · 2026-02-12

  article

  New particle formation (NPF) represents a major source of tropospheric fine aerosols. A common viewpoint is that NPF hinges thermodynamically on the volatility of condensing species and is unfavorable at high temperatures. From an intensive field campaign, we observed frequent NPF events during a heat wave. Size-resolved chemical composition of nanoparticles down to 3 nanometers was first measured, unraveling a dominant presence of carboxylic acids. Our work uncovers a spontaneous mechanism to produce supramolecular nanoparticles through self-assembly of organic acids. This discovery explains not only the unexpected NPF at high temperatures but also its ubiquitous occurrence under diverse atmospheric conditions. As global warming leads to more frequent and intense heat waves, our findings open avenues for assessing the impacts of aerosols on cloud formation, public health, and climate.

  PublisherDOI

• Abstract LB058: Investigating the role of SIM2 and SIRT3 in mitochondrial dynamics and homeostasis in ER+ breast cancer

  Cancer Research · 2025-04-25

  articleSenior author

  Abstract Mitochondrial dynamics are essential for cellular energy regulation and homeostasis, processes crucial for normal development and breast cancer progression. Maintaining mitochondrial integrity requires a balance between fusion and fission events, which influence cellular metabolism and oxidative stress responses. Recent studies have identified Singleminded-2s (SIM2s), a tumor suppressor in mammary epithelial cells, as a regulator of mitochondrial morphology and dynamics. Our data suggest that the loss of SIM2s in estrogen receptor-positive (ER+) breast cancer cells leads to altered mitochondrial morphology, with decreased mitochondrial fusion (OPA1) and increased fission (DRP1). Additionally, SIM2 loss correlates with increased acetylation of Superoxide Dismutase 2 (SOD2) at lysine residues 68 and 122, indicating reduced SIRT3 activity. These findings suggest an interaction between SIM2 and SIRT3 in regulating mitochondrial dynamics and homeostasis. Furthermore, pharmacological inhibition of SIRT3 in SIM2-deficient cells induces synthetic lethality, highlighting SIRT3 as a potential therapeutic target for metastatic breast cancer. These results emphasize a potential relationship between SIM2 and SIRT3 and their crucial roles in mitochondrial integrity and homeostasis in ER+ breast cancer. Citation Format: Hannah N. Carter, Steven W. Wall, Garhett L. Wyatt, Lilia Sanchez, Weston W. Porter. Investigating the role of SIM2 and SIRT3 in mitochondrial dynamics and homeostasis in ER+ breast cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 2 (Late-Breaking, Clinical Trial, and Invited Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_2):Abstract nr LB058.

  PublisherDOI

• Aging-induced semaphorin 7a promotes TGF-β1-mediated cell plasticity and breast tumor metastases

  Cell Reports · 2025-08-01 · 1 citations

  articleOpen access

  Breast cancer risk is transiently increased in postpartum women, and this risk is prolonged in women whose first childbirth occurs after age 30. We observe elevated semaphorin 7a (SEMA7A) in tumor tissues from patients with breast cancer aged 31-39 diagnosed <10 years after childbirth. In the aged normal murine mammary gland, transforming growth factor β+ (TGF-β+) cells have increased levels of surface SEAM7A compared to the young. TGF-β1 induces SEMA7A expression in non-transformed mammary epithelial and breast cancer cells via multiple mechanisms. In mouse mammary tumor models, we observe accelerated tumor growth and metastases, increased TGF-β+SEMA7A+ cells, and epithelial-to-mesenchymal plasticity in aged mice. SEMA7A knockout and heterozygous littermates reveal that these phenotypes depend on SEMA7A in the host. We further show SEMA7A's pro-metastatic phenotype and abrogate it via a function-blocking antibody. Collectively, these results highlight the impact aging has on the mammary gland and the risk for breast cancer tumorigenesis.

  PublisherDOI

• Loss of STING impairs lactogenic differentiation

  Development · 2024-10-01 · 1 citations

  articleOpen accessSenior author

  Heightened energetic and nutrient demand during lactogenic differentiation of the mammary gland elicits upregulation of various stress responses to support cellular homeostasis. Here, we identify the stimulator of interferon genes (STING) as an immune supporter of the functional development of mouse mammary epithelial cells (MECs). An in vitro model of MEC differentiation revealed that STING is activated in a cGAS-independent manner to produce both type I interferons and proinflammatory cytokines in response to the accumulation of mitochondrial reactive oxygen species. Induction of STING activity was found to be dependent on the breast tumor suppressor gene single-minded 2 (SIM2). Using mouse models of lactation, we discovered that loss of STING activity results in early involution of #3 mammary glands, severely impairing lactational performance. Our data suggest that STING is required for successful functional differentiation of the mammary gland and bestows a differential lactogenic phenotype between #3 mammary glands and the traditionally explored inguinal 4|9 pair. These findings affirm unique development of mammary gland pairs that is essential to consider in future investigations into normal development and breast cancer initiation.

  PublisherDOI

• Immune Cell Contribution to Mammary Gland Development

  Journal of Mammary Gland Biology and Neoplasia · 2024-08-23 · 12 citations

  reviewOpen accessSenior author

  Postpartum breast cancer (PPBC) is a unique subset of breast cancer, accounting for nearly half of the women diagnosed during their postpartum years. Mammary gland involution is widely regarded as being a key orchestrator in the initiation and progression of PPBC due to its unique wound-healing inflammatory signature. Here, we provide dialogue suggestive that lactation may also facilitate neoplastic development as a result of sterile inflammation. Immune cells are involved in all stages of postnatal mammary development. It has been proposed that the functions of these immune cells are partially directed by mammary epithelial cells (MECs) and the cytokines they produce. This suggests that a more niche area of exploration aimed at assessing activation of innate immune pathways within MECs could provide insight into immune cell contributions to the developing mammary gland. Immune cell contribution to pubertal development and mammary gland involution has been extensively studied; however, investigations into pregnancy and lactation remain limited. During pregnancy, the mammary gland undergoes dramatic expansion to prepare for lactation. As a result, MECs are susceptible to replicative stress. During lactation, mitochondria are pushed to capacity to fulfill the high energetic demands of producing milk. This replicative and metabolic stress, if unresolved, can elicit activation of innate immune pathways within differentiating MECs. In this review, we broadly discuss postnatal mammary development and current knowledge of immune cell contribution to each developmental stage, while also emphasizing a more unique area of study that will be beneficial in the discovery of novel therapeutic biomarkers of PPBC.

  PublisherOA PDFDOI

• Aging-Induced Semaphorin 7a Promotes Tgfβ1-Mediated Cell Plasticity and Breast Tumor Metastases

  SSRN Electronic Journal · 2024-01-01 · 1 citations

  preprintOpen access
  PublisherDOI

• Abstract PO5-05-08: LOSS OF SINGLEMINDED 2S RESULTS IN A PI3K SUBUNIT SWITCH WHICH DRIVES THERAPEUTIC RESISTANCE IN ESTROGEN RECEPTOR POSITIVE BREAST CANCER

  Cancer Research · 2024-05-02

  articleSenior author

  Abstract Estrogen receptor (ER) + breast cancer (BC) comprises over 70% of BC cases and are targeted via ER modulated therapies. Despite this, ER+BC patients can experience recurrence within 20 years and the majority of BC related deaths can be attributed to metastatic ER+BC. These distant metastases are commonly diagnosed as endocrine therapy resistant. Thus, there is an unmet need to identify novel biomarkers for treating ER+ patients with metastases. We have identified a tumor suppressor gene, singleminded 2s (SIM2s), expressed in breast epithelial cells that inhibits epithelial to mesenchymal transition and metastasis, and is downregulated in the progression of breast disease. In ER+BC cell lines, loss of SIM2s results in upregulation of mesenchymal markers and increased PI3K/Akt signaling. Dysregulation of the PI3K/Akt signaling pathway in ER+BC is involved with tumor progression and acquired therapeutic resistance. Our study suggests loss of SIM2s confers resistance in ER+BC through a PI3K subunit switch resulting in upregulation of pro-survival signaling. MCF7 SIM2 knock out cells exhibit increased expression of mesenchymal markers and undergo a phenotypic change compared to wild type cells. Utilizing a migration/invasion assay, MCF7 SIM2 knock out cells exemplify an increase in invasion potential compared to wild type cells. Furthermore, changes in PI3K subunit expression were observed via western blot and real time qPCR analysis. Clonogenic assays revealed an acquired resistance to PI3Kα inhibition, but a susceptibility to PI3Kδ inhibition. This is a significant finding as a current standard of care for patients with ER+ breast cancer recurrence is PI3Kα inhibition. PI3Kδ is an already approved therapeutic target in chronic lymphocytic leukemia, thus PI3Kδ may present a new therapeutically targetable opportunity for ER+BC recurrence. Elucidating the mechanism for acquired therapeutic resistance is an integral avenue for understanding how breast cancer progresses and improving the prognosis of ER+BC patients. Citation Format: Garhett Wyatt, Rachel Steinmetz, Traci Lyons, Weston Porter. LOSS OF SINGLEMINDED 2S RESULTS IN A PI3K SUBUNIT SWITCH WHICH DRIVES THERAPEUTIC RESISTANCE IN ESTROGEN RECEPTOR POSITIVE BREAST CANCER [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO5-05-08.

  PublisherDOI

• Mitochondrial structure and function adaptation in residual triple negative breast cancer cells surviving chemotherapy treatment

  Oncogene · 2023 · 77 citations

  • Biology
  • Cancer research
  • Cell biology
  DOI

• Supplementary Table 2 from Hormonal Regulation of Semaphorin 7a in ER&lt;sup&gt;+&lt;/sup&gt; Breast Cancer Drives Therapeutic Resistance

  2023-03-31

  supplementary-materialsOpen access

  &lt;p&gt;Oncomine analysis of SEMA7A expression with ER/PR biomarker status, grade, and stage&lt;/p&gt;

  PublisherOA PDFDOI

• Supplementary Table 1 from Hormonal Regulation of Semaphorin 7a in ER&lt;sup&gt;+&lt;/sup&gt; Breast Cancer Drives Therapeutic Resistance

  2023-03-31

  supplementary-materialsOpen access

  &lt;p&gt;Antibodies used for Western blots and IHC&lt;/p&gt;

  PublisherDOI

Recent grants

• NIH Grant R21CA190941

  NIH · $345k · 2017

• NIH Grant R01HD083952

  NIH · $1.5M · 2021

• NIH Grant R01CA111551

  NIH · $1.1M · 2012

• NIH Grant R21CA197896

  NIH · $355k · 2019

• NIH Grant R01ES025209

  NIH · $1.6M · 2021

Frequent coauthors

• Abraham Rothman

  University of Nevada, Las Vegas

  98 shared

• E. Tahirović

  Queen Mary University of London

  98 shared

• Jian Chen

  Tongji Hospital

  98 shared

• Liaqat Ali

  Institute for Health Metrics and Evaluation

  98 shared

• Abi Daoud

  University Hospitals of Cleveland

  98 shared

• David C. Hodgson

  98 shared

• C. McDonald

  Lincoln Medical Center

  98 shared

• Mary R. Schwartz

  Methodist Hospital

  98 shared