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  1. Article ; Online: p38 MAPK in development and cancer.

    Bradham, Cynthia / McClay, David R

    Cell cycle (Georgetown, Tex.)

    2006  Volume 5, Issue 8, Page(s) 824–828

    Abstract: ... of both embryonic development and cancer progression. This review will focus on these in vivo studies in an effort to provide ... p38 is a MAPK that has been shown to induce a wide variety of biological effects in cell culture ... evaluated in vivo, and through these studies p38 has emerged as an important regulator ...

    Abstract p38 is a MAPK that has been shown to induce a wide variety of biological effects in cell culture in response to a wide range of stimuli. These effects are dependent not only on the stimuli, but also on the cellular context, resulting in a bewildering array of possibilities. For example, p38 was shown to induce apoptosis in some cells, but prevent apoptosis in others. Similarly opposed effects had been observed with respect to cell cycle regulation. The role of p38 in inflammatory disease has been appreciated from the beginning, since it was initially identified as an cytokine inducer. More recently, p38 function has been evaluated in vivo, and through these studies p38 has emerged as an important regulator of both embryonic development and cancer progression. This review will focus on these in vivo studies in an effort to provide perspective on p38 biologically and as a pharmacological target.
    MeSH term(s) Animals ; Apoptosis ; Cell Cycle ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; Cytokines/metabolism ; Disease Progression ; Gene Expression Regulation, Developmental ; Gene Expression Regulation, Neoplastic ; Humans ; Models, Biological ; Neoplasm Metastasis ; Neoplasms/pathology ; p38 Mitogen-Activated Protein Kinases/physiology
    Chemical Substances Cytokines ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2006-04-17
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.4161/cc.5.8.2685
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5881: Show issues Location:
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  2. Article ; Online: P38 kinase in gastrointestinal cancers.

    Phan, Thuy / Zhang, Xu Hannah / Rosen, Steven / Melstrom, Laleh G

    Cancer gene therapy

    2023  Volume 30, Issue 9, Page(s) 1181–1189

    Abstract: ... proliferation, differentiation, apoptosis, stress responses and cancer development ... p38 Mitogen Activated Protein Kinases (p38 MAPKs) includes four isoforms: p38α (MAPK14), p38β (MAPK11), p38γ (MAPK12), and p38δ (MAPK13 ... transcriptional factors. Dysregulation of p38 pathways, in particular p38γ, are associated with cancer development ...

    Abstract Gastrointestinal cancers are a leading cause of cancer morbidity and mortality worldwide with 4.2 million new cases and 3.2 million deaths estimated in 2020. Despite the advances in primary and adjuvant therapies, patients still develop distant metastases and require novel therapies. Mitogen‑activated protein kinase (MAPK) cascades are crucial signaling pathways that regulate many cellular processes, including proliferation, differentiation, apoptosis, stress responses and cancer development. p38 Mitogen Activated Protein Kinases (p38 MAPKs) includes four isoforms: p38α (MAPK14), p38β (MAPK11), p38γ (MAPK12), and p38δ (MAPK13). p38 MAPK was first identified as a stress response protein kinase that phosphorylates different transcriptional factors. Dysregulation of p38 pathways, in particular p38γ, are associated with cancer development, metastasis, autophagy and tumor microenvironment. In this article, we provide an overview of p38 and p38γ with respect to gastrointestinal cancers. Furthermore, targeting p38γ is also discussed as a potential therapy for gastrointestinal cancers.
    MeSH term(s) Humans ; Mitogen-Activated Protein Kinase 11/metabolism ; Mitogen-Activated Protein Kinase 12/genetics ; Mitogen-Activated Protein Kinase 12/metabolism ; Mitogen-Activated Protein Kinase 13/metabolism ; Signal Transduction ; Gastrointestinal Neoplasms/genetics ; p38 Mitogen-Activated Protein Kinases/metabolism ; Tumor Microenvironment
    Chemical Substances Mitogen-Activated Protein Kinase 11 (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 12 (EC 2.7.1.-) ; Mitogen-Activated Protein Kinase 13 (EC 2.7.1.-) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2023-05-29
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 1212513-1
    ISSN 1476-5500 ; 0929-1903
    ISSN (online) 1476-5500
    ISSN 0929-1903
    DOI 10.1038/s41417-023-00622-1
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  3. Article ; Online: The p38 Pathway

    Adrián Martínez-Limón / Manel Joaquin / María Caballero / Francesc Posas / Eulàlia de Nadal

    International Journal of Molecular Sciences, Vol 21, Iss 6, p

    From Biology to Cancer Therapy

    2020  Volume 1913

    Abstract: ... targeting p38 in cancer and promising alternatives currently being explored. ... The p38 MAPK pathway is well known for its role in transducing stress signals from the environment ... an extensive description of the main biological functions of p38 and focus on recent studies that have ...

    Abstract The p38 MAPK pathway is well known for its role in transducing stress signals from the environment. Many key players and regulatory mechanisms of this signaling cascade have been described to some extent. Nevertheless, p38 participates in a broad range of cellular activities, for many of which detailed molecular pictures are still lacking. Originally described as a tumor-suppressor kinase for its inhibitory role in RAS-dependent transformation, p38 can also function as a tumor promoter, as demonstrated by extensive experimental data. This finding has prompted the development of specific inhibitors that have been used in clinical trials to treat several human malignancies, although without much success to date. However, elucidating critical aspects of p38 biology, such as isoform-specific functions or its apparent dual nature during tumorigenesis, might open up new possibilities for therapy with unexpected potential. In this review, we provide an extensive description of the main biological functions of p38 and focus on recent studies that have addressed its role in cancer. Furthermore, we provide an updated overview of therapeutic strategies targeting p38 in cancer and promising alternatives currently being explored.
    Keywords p38 mapk ; sapk ; phosphorylation ; oncogenicity ; tumor suppressor ; cancer treatment ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 610
    Language English
    Publishing date 2020-03-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Combined effect of chrysin and apigenin on inhibiting the development and progression of colorectal cancer by suppressing the activity of P38-MAPK/AKT pathway.

    Zhang, Xiaozhan / Zhang, Wen / Chen, Fei / Lu, Zhaohui

    IUBMB life

    2021  Volume 73, Issue 5, Page(s) 774–783

    Abstract: ... The changes of the activation of P38-MAPK/AKT pathway were evaluated underlying apigenin and chrysin ... intervention, further after co-treated with P38-MAPK agonist anisomycin. Apigenin (25 μM) combined with chrysin ... Meanwhile, p-P38 and p-AKT were significantly downregulated by chrysin and apigenin treatment. The tumor ...

    Abstract Either apigenin or chrysin alone has been found to exert anti-inflammatory and tumor suppressive effect. However, the combined effect of apigenin and chrysin on colorectal cancer (CRC) has not been fully clarified. We attempted to explore the effect of chrysin and apigenin on CRC and its related mechanism. SW480 and HCT-116 cells were treated with either apigenin or chrysin alone or two-drug combination at different doses of 5, 25, 50, 100 μM for optimal concentration determination. Then, we focused on the individual and combined effect of apigenin and chrysin on clonogenicity, apoptosis, metastasis-related behaviors of CRC cells by colony formation assay, cell scratch assay, flow cytometry, and transwell assay. The changes of the activation of P38-MAPK/AKT pathway were evaluated underlying apigenin and chrysin intervention, further after co-treated with P38-MAPK agonist anisomycin. Apigenin (25 μM) combined with chrysin (25 μM) were determined to be optimal. Treatment with the combination of apigenin (25 μM) and chrysin (25 μM) significantly reduced cell clone numbers, migration, and invasion ability, while increased the cell apoptosis in both CRC cell lines. The combined effect was higher than chrysin or apigenin alone. Meanwhile, p-P38 and p-AKT were significantly downregulated by chrysin and apigenin treatment. The tumor inhibitive effect of apigenin combined with chrysin was obviously reversed by adding P38 agonist, anisomycin. Apigenin (25 μM) combined with chrysin (25 μM) showed synergetic effect in inhibiting the growth and metastasis of CRC cells by suppressing the activity of P38-MAPK/AKT pathway.
    MeSH term(s) Adenocarcinoma/enzymology ; Adenocarcinoma/pathology ; Anisomycin/pharmacology ; Apigenin/pharmacology ; Apoptosis/drug effects ; Cell Line, Tumor ; Cell Movement/drug effects ; Clone Cells ; Colorectal Neoplasms/enzymology ; Colorectal Neoplasms/pathology ; Drug Synergism ; Flavonoids/pharmacology ; HCT116 Cells ; Humans ; MAP Kinase Signaling System/drug effects ; MAP Kinase Signaling System/physiology ; Molecular Targeted Therapy ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Neoplasm Proteins/antagonists & inhibitors ; Neoplasm Proteins/physiology ; Proto-Oncogene Proteins c-akt/physiology ; Tumor Stem Cell Assay ; p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors
    Chemical Substances Flavonoids ; Neoplasm Proteins ; chrysin (3CN01F5ZJ5) ; Anisomycin (6C74YM2NGI) ; Apigenin (7V515PI7F6) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2021-03-15
    Publishing country England
    Document type Journal Article
    ZDB-ID 1492141-8
    ISSN 1521-6551 ; 1521-6543
    ISSN (online) 1521-6551
    ISSN 1521-6543
    DOI 10.1002/iub.2456
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1611: Show issues Location:
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  5. Article ; Online: STING promotes invasion and migration of uveal melanoma through p38‑MAPK signaling.

    Zhou, Xiaoting / Meng, Fengxi / Xu, Binbin / Ma, Ruiqi / Cheng, Yun / Wu, Jihong / Qian, Jiang

    Oncology reports

    2023  Volume 51, Issue 2

    Abstract: ... migration and invasion, which the p38‑MAPK inhibitor SB203580 reversed. Finally, the results of the present ... to promote the migration and invasion of UM cells through p38‑MAPK signaling. ... upregulated the phosphorylation of p38 mitogen‑activated protein kinase (p38‑MAPK) in UM cells, enhancing cell ...

    Abstract Uveal melanoma (UM) is the most common intraocular malignant tumor in adults, with a lack of effective treatment for metastasis and a poor prognosis. Stimulator of interferon genes (STING, also known as TMEM173) plays an important role in tumor development by regulating cell proliferation, metastasis and other cellular processes. However, the function of STING in UM remains unclear and requires further investigation. The present study analyzed the expression status of STING to elucidate the mechanisms underlying UM. The correlation between STING and the prognosis of UM was evaluated based on UM RNA‑seq data and clinical information extracted from The Cancer Genome Atlas database. Quantification of STING in UM cell lines and tissues was performed using the Wes Separation protein immunoassay. The effects of STING on the proliferation, migration and invasion of UM cells were investigated using Cell Counting Kit‑8, Transwell and wound healing experiments. Survival analysis demonstrated that high levels of STING in UM tissues indicated a poor prognosis. The expression of STING in UM tissues was higher than that in the choroid membranes. Furthermore, it was found that downregulation of STING expression in UM cells suppressed migration and invasion, whereas overexpression of STING significantly promoted migration and invasion. Notably, STING had no significant effect on UM cell proliferation. It was also identified that STING positively upregulated the phosphorylation of p38 mitogen‑activated protein kinase (p38‑MAPK) in UM cells, enhancing cell migration and invasion, which the p38‑MAPK inhibitor SB203580 reversed. Finally, the results of the present study demonstrated that high STING expression in UM indicates a poor prognosis. STING was revealed to promote the migration and invasion of UM cells through p38‑MAPK signaling.
    MeSH term(s) Adult ; Humans ; Cell Line, Tumor ; Melanoma/pathology ; Uveal Neoplasms/genetics ; Uveal Neoplasms/metabolism ; Uveal Neoplasms/pathology ; MAP Kinase Signaling System/genetics ; Cell Proliferation/genetics
    Language English
    Publishing date 2023-12-15
    Publishing country Greece
    Document type Journal Article
    ZDB-ID 1222484-4
    ISSN 1791-2431 ; 1021-335X
    ISSN (online) 1791-2431
    ISSN 1021-335X
    DOI 10.3892/or.2023.8682
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    Zs.A 4213: Show issues Location:
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  6. Article ; Online: Superbinder based phosphoproteomic landscape revealed PRKCD_pY313 mediates the activation of Src and p38 MAPK to promote TNBC progression.

    Deng, Yujiao / Hou, Zhanwu / Li, Yizhen / Yi, Ming / Wu, Ying / Zheng, Yi / Yang, Fei / Zhong, Guansheng / Hao, Qian / Zhai, Zhen / Wang, Meng / Ma, Xiaobin / Kang, Huafeng / Ji, Fanpu / Dong, Chenfang / Liu, Huadong / Dai, Zhijun

    Cell communication and signaling : CCS

    2024  Volume 22, Issue 1, Page(s) 115

    Abstract: ... the aberrantly active kinases in breast cancer development and to elucidate the role of PRKCD_pY313 in triple ... signaling pathways in breast cancer, which facilitates the discovery of new oncogenic agents and drives the discovery ... of potential targets for early diagnosis and therapy of breast cancer. In this study, we have explored ...

    Abstract Phosphorylation proteomics is the basis for the study of abnormally activated kinase signaling pathways in breast cancer, which facilitates the discovery of new oncogenic agents and drives the discovery of potential targets for early diagnosis and therapy of breast cancer. In this study, we have explored the aberrantly active kinases in breast cancer development and to elucidate the role of PRKCD_pY313 in triple negative breast cancer (TNBC) progression. We collected 47 pairs of breast cancer and paired far-cancer normal tissues and analyzed phosphorylated tyrosine (pY) peptides by Superbinder resin and further enriched the phosphorylated serine/threonine (pS/pT) peptides using TiO
    MeSH term(s) Animals ; Humans ; Mice ; Cell Line, Tumor ; Cell Proliferation ; Dasatinib/pharmacology ; Mice, Nude ; p38 Mitogen-Activated Protein Kinases/metabolism ; Peptides/pharmacology ; Protein Kinase C-delta/metabolism ; Triple Negative Breast Neoplasms/drug therapy ; Triple Negative Breast Neoplasms/metabolism ; Triple Negative Breast Neoplasms/pathology ; src-Family Kinases
    Chemical Substances Dasatinib (RBZ1571X5H) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Peptides ; PRKCD protein, human (EC 2.7.11.13) ; Protein Kinase C-delta (EC 2.7.11.13) ; src-Family Kinases (EC 2.7.10.2)
    Language English
    Publishing date 2024-02-12
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2126315-2
    ISSN 1478-811X ; 1478-811X
    ISSN (online) 1478-811X
    ISSN 1478-811X
    DOI 10.1186/s12964-024-01487-z
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  7. Article ; Online: The p38 Pathway: From Biology to Cancer Therapy.

    Martínez-Limón, Adrián / Joaquin, Manel / Caballero, María / Posas, Francesc / de Nadal, Eulàlia

    International journal of molecular sciences

    2020  Volume 21, Issue 6

    Abstract: ... targeting p38 in cancer and promising alternatives currently being explored. ... The p38 MAPK pathway is well known for its role in transducing stress signals from the environment ... an extensive description of the main biological functions of p38 and focus on recent studies that have ...

    Abstract The p38 MAPK pathway is well known for its role in transducing stress signals from the environment. Many key players and regulatory mechanisms of this signaling cascade have been described to some extent. Nevertheless, p38 participates in a broad range of cellular activities, for many of which detailed molecular pictures are still lacking. Originally described as a tumor-suppressor kinase for its inhibitory role in RAS-dependent transformation, p38 can also function as a tumor promoter, as demonstrated by extensive experimental data. This finding has prompted the development of specific inhibitors that have been used in clinical trials to treat several human malignancies, although without much success to date. However, elucidating critical aspects of p38 biology, such as isoform-specific functions or its apparent dual nature during tumorigenesis, might open up new possibilities for therapy with unexpected potential. In this review, we provide an extensive description of the main biological functions of p38 and focus on recent studies that have addressed its role in cancer. Furthermore, we provide an updated overview of therapeutic strategies targeting p38 in cancer and promising alternatives currently being explored.
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Clinical Studies as Topic ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; MAP Kinase Signaling System/drug effects ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Phosphorylation ; p38 Mitogen-Activated Protein Kinases/genetics ; p38 Mitogen-Activated Protein Kinases/metabolism
    Chemical Substances Antineoplastic Agents ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2020-03-11
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms21061913
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  8. Article ; Online: Atypical p38 Signaling, Activation, and Implications for Disease.

    Burton, Jeremy C / Antoniades, William / Okalova, Jennifer / Roos, Morgan M / Grimsey, Neil J

    International journal of molecular sciences

    2021  Volume 22, Issue 8

    Abstract: The mitogen-activated protein kinase (MAPK) p38 is an essential family of kinases, regulating ... and pathophysiological conditions attributed to p38 activity, ranging from cell division and ... the adaptor protein TAB1 and p38α, driving p38 autophosphorylation independent from the classical MKK3 and ...

    Abstract The mitogen-activated protein kinase (MAPK) p38 is an essential family of kinases, regulating responses to environmental stress and inflammation. There is an ever-increasing plethora of physiological and pathophysiological conditions attributed to p38 activity, ranging from cell division and embryonic development to the control of a multitude of diseases including retinal, cardiovascular, and neurodegenerative diseases, diabetes, and cancer. Despite the decades of intense investigation, a viable therapeutic approach to disrupt p38 signaling remains elusive. A growing body of evidence supports the pathological significance of an understudied atypical p38 signaling pathway. Atypical p38 signaling is driven by a direct interaction between the adaptor protein TAB1 and p38α, driving p38 autophosphorylation independent from the classical MKK3 and MKK6 pathways. Unlike the classical MKK3/6 signaling pathway, atypical signaling is selective for just p38α, and at present has only been characterized during pathophysiological stimulation. Recent studies have linked atypical signaling to dermal and vascular inflammation, myocardial ischemia, cancer metastasis, diabetes, complications during pregnancy, and bacterial and viral infections. Additional studies are required to fully understand how, when, where, and why atypical p38 signaling is induced. Furthermore, the development of selective TAB1-p38 inhibitors represents an exciting new opportunity to selectively inhibit pathological p38 signaling in a wide array of diseases.
    MeSH term(s) Animals ; Cardiovascular Diseases/metabolism ; Communicable Diseases/metabolism ; Humans ; MAP Kinase Signaling System ; Neurodegenerative Diseases/metabolism ; p38 Mitogen-Activated Protein Kinases/metabolism
    Chemical Substances p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2021-04-17
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms22084183
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  9. Article ; Online: Role of p38 MAP kinase in cancer stem cells and metastasis.

    Kudaravalli, Sriya / den Hollander, Petra / Mani, Sendurai A

    Oncogene

    2022  Volume 41, Issue 23, Page(s) 3177–3185

    Abstract: ... stem cells (CSCs) underlie treatment resistance and metastasis. p38 mitogen-activated protein kinase (p38 MAPK) is ... approaches targeting p38 can sensitize tumors to chemotherapy and prevent metastatic progression. ... Therapeutic resistance and metastatic progression are responsible for the majority of cancer ...

    Abstract Therapeutic resistance and metastatic progression are responsible for the majority of cancer mortalities. In particular, the development of resistance is a significant barrier to the efficacy of cancer treatments such as chemotherapy, radiotherapy, targeted therapies, and immunotherapies. Cancer stem cells (CSCs) underlie treatment resistance and metastasis. p38 mitogen-activated protein kinase (p38 MAPK) is downstream of several CSC-specific signaling pathways, and it plays an important role in CSC development and maintenance and contributes to metastasis and chemoresistance. Therefore, the development of therapeutic approaches targeting p38 can sensitize tumors to chemotherapy and prevent metastatic progression.
    MeSH term(s) Humans ; MAP Kinase Signaling System ; Mitogen-Activated Protein Kinase 14/metabolism ; Neoplasms/metabolism ; Neoplastic Stem Cells/pathology ; Signal Transduction ; p38 Mitogen-Activated Protein Kinases/genetics ; p38 Mitogen-Activated Protein Kinases/metabolism
    Chemical Substances Mitogen-Activated Protein Kinase 14 (EC 2.7.11.24) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2022-04-30
    Publishing country England
    Document type Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/s41388-022-02329-3
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    Zs.A 2218: Show issues Location:
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  10. Article ; Online: ZIP14 Affects the Proliferation, Apoptosis, and Migration of Cervical Cancer Cells by Regulating the P38 MAPK Pathway.

    Jiang, Lixia / Xie, Ting / Xia, Yu / Li, Feng / Zhong, Tianyu / Lai, Mi

    Current cancer drug targets

    2023  

    Abstract: ... pathway analysis revealed the potential involvement of the P38 mitogen-activated protein kinase (MAPK ... pathway in CC pathogenesis. Overexpression of ZIP14 in HeLa and Caski cells increased p38 phosphorylation ... Importantly, the bioeffects induced by ZIP14 overexpression could be counteracted by the p38 MAPK pathway ...

    Abstract Background: Cervical cancer (CC) remains a major public health concern and is a leading cause of female mortality worldwide. Understanding the molecular basis of its pathogenesis is essential for the development of novel therapeutic strategies. In this study, we aimed to dissect the role of a specific molecule, ZIP14, in the initiation and progression of CC.
    Method: We used Gene Expression Omnibus for target gene identification, while KEGG was used to delineate CC-related pathways. Proliferation, migration, and apoptosis levels in CC cells were assessed using CCK8, Transwell, and flow cytometry, respectively. The effect of the target genes on the in vivo tumorigenesis of CC cells was evaluated using the subcutaneous tumorigenesis assay.
    Results: ZIP14 (SLC39A14) was found to be underexpressed in CC samples. Our KEGG pathway analysis revealed the potential involvement of the P38 mitogen-activated protein kinase (MAPK) pathway in CC pathogenesis. Overexpression of ZIP14 in HeLa and Caski cells increased p38 phosphorylation, inhibited cell growth and migration, and enhanced apoptosis. Conversely, ZIP14 knockdown produced the opposite effects. Importantly, the bioeffects induced by ZIP14 overexpression could be counteracted by the p38 MAPK pathway inhibitor SB203580. In vivo experiments further confirmed the influence of ZIP14 on CC cell migration.
    Conclusion: Our study is the first to elucidate the pivotal role of ZIP14 in the pathogenesis of CC, revealing its inhibitory effects through the activation of the p38 MAPK signaling pathway. The discovery not only provides a deeper understanding of CC's molecular underpinnings, but also highlights ZIP14 as a promising therapeutic target. As ZIP14 holds significant potential for therapeutic interventions, our findings lay a robust foundation for further studies and pave the way for the exploration of novel treatment modalities for cervical cancer.
    Language English
    Publishing date 2023-11-21
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2064824-8
    ISSN 1873-5576 ; 1568-0096
    ISSN (online) 1873-5576
    ISSN 1568-0096
    DOI 10.2174/0115680096250711231024063841
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