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  1. Article ; Online: Acute respiratory distress syndrome enhances tumor metastasis into lungs: Role of BRD4 in the tumor microenvironment.

    Pooladanda, Venkatesh / Thatikonda, Sowjanya / Priya Muvvala, Sai / Godugu, Chandraiah

    International immunopharmacology

    2023  Volume 115, Page(s) 109701

    Abstract: Acute respiratory distress syndrome (ARDS) is associated with severe lung inflammation, edema, hypoxia, and high vascular permeability. The COVID-19-associated pandemic ARDS caused by SARS-CoV-2 has created dire global conditions and has been highly ... ...

    Abstract Acute respiratory distress syndrome (ARDS) is associated with severe lung inflammation, edema, hypoxia, and high vascular permeability. The COVID-19-associated pandemic ARDS caused by SARS-CoV-2 has created dire global conditions and has been highly contagious. Chronic inflammatory disease enhances cancer cell proliferation, progression, and invasion. We investigated how acute lung inflammation activates the tumor microenvironment and enhances lung metastasis in LPS induced in vitro and in vivo models. Respiratory illness is mainly caused by cytokine storm, which further influences oxidative and nitrosative stress. The LPS-induced inflammatory cytokines made the conditions suitable for the tumor microenvironment in the lungs. In the present study, we observed that LPS induced the cytokine storm and promoted lung inflammation via BRD4, which further caused the nuclear translocation of p65 NF-κB and STAT3. The transcriptional activation additionally triggers the tumor microenvironment and lung metastasis. Thus, BRD4-regulated p65 and STAT3 transcriptional activity in ARDS enhances lung tumor metastasis. Moreover, LPS-induced ARDS might promote the tumor microenvironment and increase cancer metastasis into the lungs. Collectively, BRD4 plays a vital role in inflammation-mediated tumor metastasis and is found to be a diagnostic and molecular target in inflammation-associated cancers.
    MeSH term(s) Humans ; Nuclear Proteins/genetics ; Lipopolysaccharides/pharmacology ; Tumor Microenvironment ; Cytokine Release Syndrome ; COVID-19 ; SARS-CoV-2 ; Transcription Factors/genetics ; Lung/pathology ; Respiratory Distress Syndrome/chemically induced ; Pneumonia/chemically induced ; Inflammation ; Lung Neoplasms ; Cell Cycle Proteins/genetics
    Chemical Substances Nuclear Proteins ; Lipopolysaccharides ; Transcription Factors ; BRD4 protein, human ; Cell Cycle Proteins
    Language English
    Publishing date 2023-01-09
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2043785-7
    ISSN 1878-1705 ; 1567-5769
    ISSN (online) 1878-1705
    ISSN 1567-5769
    DOI 10.1016/j.intimp.2023.109701
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    Zs.A 5408: Show issues Location:
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  2. Article ; Online: Niclosamide inhibits epithelial-mesenchymal transition with apoptosis induction in BRAF/ NRAS mutated metastatic melanoma cells.

    Thatikonda, Sowjanya / Pooladanda, Venkatesh / Tokala, Ramya / Nagula, Shankaraiah / Godugu, Chandraiah

    Toxicology in vitro : an international journal published in association with BIBRA

    2023  Volume 89, Page(s) 105579

    Abstract: Malignant melanoma is considered a deadly aggressive form of skin cancer that frequently metastasizes to various distal organs, which harbors mutations of the BRAF or NRAS which occur in 30 to 50% of melanoma patients. The growth factors secreted by ... ...

    Abstract Malignant melanoma is considered a deadly aggressive form of skin cancer that frequently metastasizes to various distal organs, which harbors mutations of the BRAF or NRAS which occur in 30 to 50% of melanoma patients. The growth factors secreted by melanoma cells contribute to tumor angiogenesis with the acquisition of metastatic potential by epithelial-mesenchymal transition (EMT) and drive melanoma growth toward a more aggressive form. Niclosamide (NCL) is an FDA-approved anthelmintic drug and is reported to have strong anti-cancer properties against various solid and liquid tumors. Its role in BRAF or NRAS mutated cells is unknown. In this context, we uncovered the role of NCL in impeding malignant metastatic melanoma in vitro in SK-MEL-2 and SK-MEL-28 cell lines. We found that NCL induces significant ROS generation and apoptosis through a series of molecular mechanisms, such as depolarization of mitochondrial membrane potential, arresting the cell cycle at the sub G1 phase with a significant increase in the DNA cleavage via topoisomerase II in both cell lines. We also found that NCL potently inhibited metastasis, which was examined by scratch wound assay, Additionally, we found that NCL inhibits the most important markers involved in the EMT signaling cascade that are stimulated by TGF-β such as N-cadherin, Snail, Slug, Vimentin, α-SMA and p-Smad 2/3. This work provides useful insights into the mechanism of NCL in BRAF/NRAF mutant melanoma cells via inhibition of molecular signaling events involved in EMT signaling, and apoptosis induction.
    MeSH term(s) Humans ; Proto-Oncogene Proteins B-raf/genetics ; Niclosamide/pharmacology ; Epithelial-Mesenchymal Transition ; Melanoma/drug therapy ; Melanoma/genetics ; Melanoma/metabolism ; Apoptosis ; Cell Line, Tumor ; Mutation ; Membrane Proteins/genetics ; GTP Phosphohydrolases/genetics
    Chemical Substances Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; Niclosamide (8KK8CQ2K8G) ; BRAF protein, human (EC 2.7.11.1) ; NRAS protein, human (EC 3.6.1.-) ; Membrane Proteins ; GTP Phosphohydrolases (EC 3.6.1.-)
    Language English
    Publishing date 2023-03-03
    Publishing country England
    Document type Journal Article
    ZDB-ID 639064-x
    ISSN 1879-3177 ; 0887-2333
    ISSN (online) 1879-3177
    ISSN 0887-2333
    DOI 10.1016/j.tiv.2023.105579
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  3. Article ; Online: The current understanding and potential therapeutic options to combat COVID-19.

    Pooladanda, Venkatesh / Thatikonda, Sowjanya / Godugu, Chandraiah

    Life sciences

    2020  Volume 254, Page(s) 117765

    Abstract: The ongoing wreaking global outbreak of the novel human beta coronavirus (CoV) pathogen was presumed to be from a seafood wholesale market in Wuhan, China, belongs to the Coronaviridae family in the Nidovirales order. The virus is highly contagious with ... ...

    Abstract The ongoing wreaking global outbreak of the novel human beta coronavirus (CoV) pathogen was presumed to be from a seafood wholesale market in Wuhan, China, belongs to the Coronaviridae family in the Nidovirales order. The virus is highly contagious with potential human-human transmission which was named as the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has spread across six continents and emerged as a global pandemic in short span with alarming levels of spread and severity. This virus associated symptoms and infectious respiratory illness is designated as coronavirus disease 19 (COVID-19). The SARS-CoV-2 possesses enveloped club-like spike protein projections with positive-sense large RNA genome and has a unique replication strategy. This virus was believed to have zoonotic origin with genetical identity to bat and pangolin CoV. In the current review, we introduce a general overview about the human CoVs and the associated diseases, the origin, structure, replication and key clinical events that occur in the COVID-19 pathogenicity. Furthermore, we focused on possible therapeutic options such as repurposing drugs including antimalarials, antivirals, antiparasitic drugs, and anti-HIV drugs, as well as monoclonal antibodies, vaccines as potential treatment options. Also we have summarized the latest research progress on the usage of stem cell therapy, human convalescent serum, interferon's, in the treatment of COVID-19.
    MeSH term(s) Animals ; Betacoronavirus/isolation & purification ; COVID-19 ; Coronavirus Infections/epidemiology ; Coronavirus Infections/therapy ; Coronavirus Infections/virology ; Pandemics/prevention & control ; Pneumonia, Viral/epidemiology ; Pneumonia, Viral/therapy ; Pneumonia, Viral/virology ; SARS-CoV-2 ; Zoonoses/epidemiology ; Zoonoses/therapy ; Zoonoses/virology
    Keywords covid19
    Language English
    Publishing date 2020-05-08
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 3378-9
    ISSN 1879-0631 ; 0024-3205
    ISSN (online) 1879-0631
    ISSN 0024-3205
    DOI 10.1016/j.lfs.2020.117765
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  4. Article ; Online: Selenium nanoparticles produce a beneficial effect in psoriasis by reducing epidermal hyperproliferation and inflammation.

    Gangadevi, Vinod / Thatikonda, Sowjanya / Pooladanda, Venkatesh / Devabattula, Geetanjali / Godugu, Chandraiah

    Journal of nanobiotechnology

    2021  Volume 19, Issue 1, Page(s) 101

    Abstract: Background: Psoriasis is a chronic autoimmune skin disease characterized by hyperproliferation of keratinocytes. Wide treatment options used to treat psoriasis is associated with various adverse effects. To overcome this nanoformulation is prepared. ... ...

    Abstract Background: Psoriasis is a chronic autoimmune skin disease characterized by hyperproliferation of keratinocytes. Wide treatment options used to treat psoriasis is associated with various adverse effects. To overcome this nanoformulation is prepared. Selenium is an essential trace element and plays major role in oxidation reduction system. Toxicity and stability limits the applications of selenium. Toxicity can be reduced and stabilized upon preparation into nanoparticles.
    Results: Selenium nanoparticles (SeNPs) exhibit potent apoptosis through the generation of reactive oxygen species (ROS) with cell cycle arrest. SeNPs topical gel application produced significant attenuation of psoriatic severity with the abrogation of acanthosis and splenomegaly. SeNPs reduced the phosphorylation and expressions of MAPKs, STAT3, GSK-3β, Akt along with PCNA, Ki67, and cyclin-D1.
    Conclusion: SeNPs inhibit various inflammation and proliferation mediated pathways and could be an ideal candidate for psoriasis therapy.
    Materials and methods: SeNPs were characterized and various techniques were used to determine apoptosis and other molecular mechanisms. In vivo studies were performed by inducing psoriasis with imiquimod (IMQ). SeNPs were administered via topical route.
    MeSH term(s) Animals ; Apoptosis/drug effects ; Cell Cycle Checkpoints ; Cell Line ; Glycogen Synthase Kinase 3 beta/metabolism ; Humans ; Imiquimod ; Inflammation/drug therapy ; Keratinocytes ; Mice ; Mice, Inbred BALB C ; Nanoparticles/chemistry ; Nanoparticles/therapeutic use ; Oxidation-Reduction ; Phosphorylation ; Psoriasis/drug therapy ; Reactive Oxygen Species ; STAT3 Transcription Factor/metabolism ; Selenium/chemistry ; Selenium/pharmacology
    Chemical Substances Reactive Oxygen Species ; STAT3 Transcription Factor ; STAT3 protein, human ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; Selenium (H6241UJ22B) ; Imiquimod (P1QW714R7M)
    Language English
    Publishing date 2021-04-13
    Publishing country England
    Document type Journal Article
    ISSN 1477-3155
    ISSN (online) 1477-3155
    DOI 10.1186/s12951-021-00842-3
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  5. Article ; Online: Repurposing an old drug for new use: Niclosamide in psoriasis-like skin inflammation.

    Thatikonda, Sowjanya / Pooladanda, Venkatesh / Godugu, Chandraiah

    Journal of cellular physiology

    2019  Volume 235, Issue 6, Page(s) 5270–5283

    Abstract: Drug discovery is an onerous, extremely expensive, and time-consuming process. Instead, drug repurposing is an attractive strategy for exploiting novel indications for a drug beyond its original use. The untapped potential of drug repurposing compensates ...

    Abstract Drug discovery is an onerous, extremely expensive, and time-consuming process. Instead, drug repurposing is an attractive strategy for exploiting novel indications for a drug beyond its original use. The untapped potential of drug repurposing compensates the barriers associated with the drug discovery pipeline. Psoriasis is an autoimmune skin disease, where hyperproliferation of keratinocytes and exaggerated immune responses are the important hallmarks of the disease. Extensive in vitro and preclinical research has demonstrated that niclosamide was found to exert potent anticancer and anti-inflammatory properties by targeting STAT3, p65 NF-κB, and NFATc-1 signaling paradigm with minimal host toxicity. From the disease perspective, the static intracellular molecular network in both cancer and psoriasis share overlapping pathological features in terms of hyperproliferation and chronic inflammation, which is mediated by the aforementioned signaling cascade. The plausible mechanistic relevance has prompted us to investigate the implementation of niclosamide for repositioning in psoriasis. Our in vitro and in vivo findings suggest that niclosamide inhibits keratinocytes hyperproliferation by reactive oxygen species-mediated apoptosis through the loss of mitochondrial membrane potential, cell cycle arrest at Sub G1 phase, and DNA fragmentation. Furthermore, niclosamide treatment resulted in abrogation of lipopolysaccharide-induced inflammatory cytokine levels in murine macrophages. Additionally, our results provided a preclinical rationale in imiquimod (IMQ)-induced BALB/c mouse model, where niclosamide diligently mitigated the IMQ-induced epidermal hyperplasia and inflammation by downregulating STAT3, p65 NF-κB, and NFATc-1 transcription factors along with Akt, Ki-67, and ICAM-1 protein expression.
    MeSH term(s) Animals ; Anti-Inflammatory Agents/pharmacology ; Apoptosis/drug effects ; Drug Repositioning ; Humans ; Inflammation/chemically induced ; Inflammation/drug therapy ; Inflammation/pathology ; Keratinocytes/drug effects ; Lipopolysaccharides/toxicity ; Mice ; Mice, Inbred BALB C ; NFATC Transcription Factors/genetics ; Niclosamide/pharmacology ; Psoriasis/drug therapy ; Psoriasis/pathology ; STAT3 Transcription Factor/genetics ; Signal Transduction/drug effects ; Skin Diseases/drug therapy ; Skin Diseases/pathology ; Transcription Factor RelA/genetics
    Chemical Substances Anti-Inflammatory Agents ; Lipopolysaccharides ; NFATC Transcription Factors ; Nfatc1 protein, mouse ; Rela protein, mouse ; STAT3 Transcription Factor ; Stat3 protein, mouse ; Transcription Factor RelA ; Niclosamide (8KK8CQ2K8G)
    Language English
    Publishing date 2019-12-17
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3116-1
    ISSN 1097-4652 ; 0021-9541
    ISSN (online) 1097-4652
    ISSN 0021-9541
    DOI 10.1002/jcp.29413
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    Uc I Zs.212: Show issues Location:
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  6. Article ; Online: Piperlongumine regulates epigenetic modulation and alleviates psoriasis-like skin inflammation via inhibition of hyperproliferation and inflammation.

    Thatikonda, Sowjanya / Pooladanda, Venkatesh / Sigalapalli, Dilep Kumar / Godugu, Chandraiah

    Cell death & disease

    2020  Volume 11, Issue 1, Page(s) 21

    Abstract: Psoriasis is an autoimmune skin disease, where chronic immune responses due to exaggerated cytokine signaling, abnormal differentiation, and evasion of keratinocytes apoptosis plays a crucial role in mediating abnormal keratinocytes hyperproliferation. ... ...

    Abstract Psoriasis is an autoimmune skin disease, where chronic immune responses due to exaggerated cytokine signaling, abnormal differentiation, and evasion of keratinocytes apoptosis plays a crucial role in mediating abnormal keratinocytes hyperproliferation. From the therapeutic perspective, the molecules with strong anti-proliferative and anti-inflammatory properties could have tremendous relevance. In this study, we demonstrated that piperlongumine (PPL) treatment effectively abrogated the hyperproliferation and differentiation of keratinocytes by inducing ROS-mediated late apoptosis with loss of mitochondrial membrane potential. Besides, the arrest of cell cycle was found at Sub-G1 phase as a result of DNA fragmentation. Molecularly, inhibition of STAT3 and Akt signaling was observed with a decrease in proliferative markers such as PCNA, ki67, and Cyclin D1 along with anti-apoptotic Bcl-2 protein expression. Keratin 17 is a critical regulator of keratinocyte differentiation, and it was found to be downregulated with PPL significantly. Furthermore, prominent anti-inflammatory effects were observed by inhibition of lipopolysaccharide (LPS)/Imiquimod (IMQ)-induced p65 NF-κB signaling cascade and strongly inhibited the production of cytokine storm involved in psoriasis-like skin inflammation, thus led to the restoration of normal epidermal architecture with reduction of epidermal hyperplasia and splenomegaly. In addition, PPL epigenetically inhibited histone-modifying enzymes, which include histone deacetylases (HDACs) of class I (HDAC1-4) and class II (HDAC6) evaluated by immunoblotting and HDAC enzyme assay kit. In addition, our results show that PPL effectively inhibits the nuclear translocation of p65 and a histone modulator HDAC3, thus sequestered in the cytoplasm of macrophages. Furthermore, PPL effectively enhanced the protein-protein interactions of HDAC3 and p65 with IκBα, which was disrupted by LPS stimulation and were evaluated by Co-IP and molecular modeling. Collectively, our findings indicate that piperlongumine may serve as an anti-proliferative and anti-inflammatory agent and could serve as a potential therapeutic option in treating psoriasis.
    MeSH term(s) Animals ; Apoptosis/drug effects ; Cell Proliferation/drug effects ; Chemokines/metabolism ; Dioxolanes/pharmacology ; Dioxolanes/therapeutic use ; Epidermis/pathology ; Epigenesis, Genetic/drug effects ; HaCaT Cells ; Histone Deacetylase Inhibitors/pharmacology ; Histone Deacetylases/metabolism ; Histones/metabolism ; Humans ; Imiquimod/adverse effects ; Inflammation/drug therapy ; Inflammation/genetics ; Keratin-17/metabolism ; Keratinocytes/drug effects ; Keratinocytes/pathology ; Lipopolysaccharides ; Mice ; Mice, Inbred BALB C ; Models, Biological ; Phosphorylation/drug effects ; Protein Binding/drug effects ; Psoriasis/chemically induced ; Psoriasis/drug therapy ; Psoriasis/genetics ; Psoriasis/pathology ; RAW 264.7 Cells ; STAT3 Transcription Factor/metabolism ; Skin/pathology
    Chemical Substances Chemokines ; Dioxolanes ; Histone Deacetylase Inhibitors ; Histones ; Keratin-17 ; Lipopolysaccharides ; STAT3 Transcription Factor ; Histone Deacetylases (EC 3.5.1.98) ; histone deacetylase 3 (EC 3.5.1.98) ; piperlongumine (SGD66V4SVJ) ; Imiquimod (P1QW714R7M)
    Language English
    Publishing date 2020-01-10
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/s41419-019-2212-y
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  7. Article ; Online: The current understanding and potential therapeutic options to combat COVID-19

    Pooladanda, Venkatesh / Thatikonda, Sowjanya / Godugu, Chandraiah

    Life Sciences

    2020  Volume 254, Page(s) 117765

    Keywords General Pharmacology, Toxicology and Pharmaceutics ; General Biochemistry, Genetics and Molecular Biology ; General Medicine ; covid19
    Language English
    Publisher Elsevier BV
    Publishing country us
    Document type Article ; Online
    ZDB-ID 3378-9
    ISSN 1879-0631 ; 0024-3205
    ISSN (online) 1879-0631
    ISSN 0024-3205
    DOI 10.1016/j.lfs.2020.117765
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  8. Article ; Online: BRD4 targeting nanotherapy prevents lipopolysaccharide induced acute respiratory distress syndrome.

    Pooladanda, Venkatesh / Thatikonda, Sowjanya / Muvvala, Sai Priya / Devabattula, Geetanjali / Godugu, Chandraiah

    International journal of pharmaceutics

    2021  Volume 601, Page(s) 120536

    Abstract: Acute respiratory distress syndrome (ARDS) is a life threatening respiratory disease associated with pulmonary edema, alveolar dysfunction, hypoxia, and inflammatory cell accumulation. The most contagious form of COVID-19 associated with ARDS caused by ... ...

    Abstract Acute respiratory distress syndrome (ARDS) is a life threatening respiratory disease associated with pulmonary edema, alveolar dysfunction, hypoxia, and inflammatory cell accumulation. The most contagious form of COVID-19 associated with ARDS caused by SARS-CoV-2. SARS-CoV-2 majorly produces the cytokine storm and severe lung inflammation and ultimately leads to respiratory failure. ARDS is a complex disease and there is no proper therapeutics for effective therapy. Still, there is a huge scope to identify novel targets to combat respiratory illness. In the current study, we have identified the epigenetic regulating protein BRD4 and developed siRNA based nanomedicine to treat the ARDS. The liposomes were prepared by thin-film hydration method, where BRD4 siRNA complexed with cationic lipid and exhibited 96.24 ± 18.01 nm size and stable even in the presence of RNase. BRD4 siRNA lipoplexes (BRD4-siRNA-LP) inhibited inflammatory cells in lungs and suppressed the lipopolysaccharide (LPS) induced the neutrophil infiltration and mast cell accumulation. Also, BRD4 siRNA based nanomedicine significantly reduced the LPS induced cytokine storm followed by inflammatory signaling pathways. Interestingly, BRD4-siRNA-LP suppressed the LPS-induced p65 and STAT3 nuclear translocation and ameliorated the lung inflammation. Thus, BRD4-siRNA-LP could be a plausible therapeutic option for treating ARDS and might be useful for combating the COVID-19 associated respiratory illness.
    MeSH term(s) COVID-19 ; Cell Cycle Proteins ; Humans ; Lipopolysaccharides ; Nuclear Proteins ; Respiratory Distress Syndrome/drug therapy ; SARS-CoV-2 ; Transcription Factors/genetics
    Chemical Substances BRD4 protein, human ; Cell Cycle Proteins ; Lipopolysaccharides ; Nuclear Proteins ; Transcription Factors
    Language English
    Publishing date 2021-03-27
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 428962-6
    ISSN 1873-3476 ; 0378-5173
    ISSN (online) 1873-3476
    ISSN 0378-5173
    DOI 10.1016/j.ijpharm.2021.120536
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  9. Article: An Adaptogen: Withaferin A Ameliorates

    Bale, Swarna / Venkatesh, Pooladanda / Sunkoju, Manoj / Godugu, Chandraiah

    Frontiers in pharmacology

    2018  Volume 9, Page(s) 248

    Abstract: Pulmonary fibrosis (PF) is chronic lung disease with only two FDA approved clinically available drugs, with limited safety profile. Inadequate therapy motivated us to explore the effect of vimentin inhibitor Withaferin A, as an anti-fibrotic agent ... ...

    Abstract Pulmonary fibrosis (PF) is chronic lung disease with only two FDA approved clinically available drugs, with limited safety profile. Inadequate therapy motivated us to explore the effect of vimentin inhibitor Withaferin A, as an anti-fibrotic agent against TGF-β1-induced
    Language English
    Publishing date 2018-03-22
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2018.00248
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  10. Article ; Online: Sialyl-Tn serves as a potential therapeutic target for ovarian cancer.

    Al-Alem, Linah / Prendergast, Jillian M / Clark, Justin / Zarrella, Bianca / Zarrella, Dominique T / Hill, Sarah J / Growdon, Whitfield B / Pooladanda, Venkatesh / Spriggs, David R / Cramer, Daniel / Elias, Kevin M / Nazer, Rawan I / Skates, Steven J / Behrens, Jeff / Dransfield, Daniel T / Rueda, Bo R

    Journal of ovarian research

    2024  Volume 17, Issue 1, Page(s) 71

    Abstract: Background: Ovarian cancer remains the deadliest of the gynecologic cancers in the United States. There have been limited advances in treatment strategies that have seen marked increases in overall survival. Thus, it is essential to continue developing ... ...

    Abstract Background: Ovarian cancer remains the deadliest of the gynecologic cancers in the United States. There have been limited advances in treatment strategies that have seen marked increases in overall survival. Thus, it is essential to continue developing and validating new treatment strategies and markers to identify patients who would benefit from the new strategy. In this report, we sought to further validate applications for a novel humanized anti-Sialyl Tn antibody-drug conjugate (anti-STn-ADC) in ovarian cancer.
    Methods: We aimed to further test a humanized anti-STn-ADC in sialyl-Tn (STn) positive and negative ovarian cancer cell line, patient-derived organoid (PDO), and patient-derived xenograft (PDX) models. Furthermore, we sought to determine whether serum STn levels would reflect STn positivity in the tumor samples enabling us to identify patients that an anti-STn-ADC strategy would best serve. We developed a custom ELISA with high specificity and sensitivity, that was used to assess whether circulating STn levels would correlate with stage, progression-free survival, overall survival, and its value in augmenting CA-125 as a diagnostic. Lastly, we assessed whether the serum levels reflected what was observed via immunohistochemical analysis in a subset of tumor samples.
    Results: Our in vitro experiments further define the specificity of the anti-STn-ADC. The ovarian cancer PDO, and PDX models provide additional support for an anti-STn-ADC-based strategy for targeting ovarian cancer. The custom serum ELISA was informative in potential triaging of patients with elevated levels of STn. However, it was not sensitive enough to add value to existing CA-125 levels for a diagnostic. While the ELISA identified non-serous ovarian tumors with low CA-125 levels, the sample numbers were too small to provide any confidence the STn ELISA would meaningfully add to CA-125 for diagnosis.
    Conclusions: Our preclinical data support the concept that an anti-STn-ADC may be a viable option for treating patients with elevated STn levels. Moreover, our STn-based ELISA could complement IHC in identifying patients with whom an anti-STn-based strategy might be more effective.
    MeSH term(s) Humans ; Female ; Antigens, Tumor-Associated, Carbohydrate/metabolism ; CA-125 Antigen ; Ovarian Neoplasms ; Genital Neoplasms, Female ; Enzyme-Linked Immunosorbent Assay ; Biomarkers, Tumor
    Chemical Substances Antigens, Tumor-Associated, Carbohydrate ; CA-125 Antigen ; Biomarkers, Tumor
    Language English
    Publishing date 2024-04-02
    Publishing country England
    Document type Journal Article
    ZDB-ID 2455679-8
    ISSN 1757-2215 ; 1757-2215
    ISSN (online) 1757-2215
    ISSN 1757-2215
    DOI 10.1186/s13048-024-01397-1
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