ArticleCancer medicine2019
CRM197 reverses paclitaxel resistance by inhibiting the NAC-1/Gadd45 pathway in paclitaxel-resistant ovarian cancer cells.
Article in Cancer medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- NAC1/ACOX2 Axis as a Novel Therapeutic Target for Endometriosis-Related Ovarian Neoplasms.International journal of molecular sciences · 2025Article
- AHNAK2 confers 5-fluorouracil resistance in colorectal cancer via activation of the AKT/GSK-3β signaling axis.Clinical and experimental medicine · 2025Article
- NACC1 accelerates the progression of AML by regulating the ADAM9/PI3K/AKT axis.International journal of medical sciences · 2025Article
- Mechanisms of the JNK/p38 MAPK signaling pathway in drug resistance in ovarian cancer.Frontiers in oncology · 2025Review
- The Multiple Functions of HB-EGF in Female Reproduction and Related Cancer: Molecular Mechanisms and Targeting Strategies.Reproductive sciences (Thousand Oaks, Calif.) · 2024Review
- ANGPTL3 diminishes the resistance of ovarian cancer to paclitaxel by blocking the PI3K-AKT-mTOR signaling pathway.Heliyon · 2024Article
- Identification of Copper Homeostasis-Related Gene Signature for Predicting Prognosis in Patients with Epithelial Ovarian Cancer.Cancer informatics · 2024Article
- GADD45α alleviates the CDDP resistance of SK-OV3/cddp cells via redox-mediated DNA damage.Oncology letters · 2021Article
- Integrated microRNA and mRNA signatures associated with overall survival in epithelial ovarian cancer.PloS one · 2021Article
- GADD45B Facilitates Metastasis of Ovarian Cancer Through Epithelial-Mesenchymal Transition.OncoTargets and therapy · 2021Article
- CRM197 reverses paclitaxel resistance by inhibiting the NAC-1/Gadd45 pathway in paclitaxel-resistant ovarian cancer cells.Cancer medicine · 2019Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Heparin-binding epidermal growth factor-like growth factor (HB-EGF) is a new promising target for the treatment of ovarian cancer. Our previous study showed that cross-reacting material 197 (CRM197), a specific HB-EGF inhibitor, significantly reverses resistance against paclitaxel in paclitaxel-resistant ovarian cancer cells. However, the mechanism of the effect of CRM197 on the reversion of paclitaxel resistance was unclear. In this study, in vitro and in vivo data suggested that CRM197 treatment sensitized paclitaxel-resistant ovarian cancer cells to paclitaxel, at least in part, via nucleus accumbens-1 (NAC-1) and its downstream pathway, DNA damage-inducible 45-γ interacting protein (Gadd45gip1)/growth arrest and DNA damage-inducible 45 (Gadd45), in A2780/Taxol and SKOV3/Taxol cells. The results also showed that CRM197 activated the proapoptotic JNK/p38MAPK pathway to enhance caspase-3 activity and apoptosis by downregulation of the NAC-1/Gadd45gip1/Gadd45 pathway, leading to reversion of paclitaxel resistance in A2780/Taxol and SKOV3/Taxol cells. This study provides the first mechanism through which CRM197 significantly reverses resistance against paclitaxel by modulating the NAC-1/Gadd45gip1/Gadd45 pathway in paclitaxel-resistant ovarian cancer cells, and the mechanism of HB-EGF inhibition as a novel therapeutic strategy for patients with paclitaxel-resistant ovarian cancer.
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