p38 Mitogen-activated protein kinase modulates cisplatin resistance in Head and Neck Squamous Cell Carcinoma cells

Roy, Shomereeta; S, Roy; Anuja, Kumari; Thakur, Shilpa; Akhter, Yusuf; Padhi, Swatishree; Banerjee, Birendranath

doi:10.1016/j.archoralbio.2020.104981

Cited by 12 publications

(10 citation statements)

References 27 publications

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“…Furthermore, inhibition of p38 in cisplatin‐resistant HNSCC cells reduced the expression of cancer stem cell makers, β‐catenin, migration and sphere formation ability along with increased apoptotic index, and sensitizes these resistant cells to cisplatin. In conclusion, the study suggested that inactivation of p38 MAPK could improve the efficacy of chemotherapy in drug‐resistant HNSCC 37 . Our experimental result that 7‐Epitaxol can reduce p38 expression and further increase therapeutic efficacy in cis‐resistant HNSCC cells could be confirmed by these previous studies.…”

Section: Discussionsupporting

confidence: 78%

7‐Epitaxol induces apoptosis in cisplatin‐resistant head and neck squamous cell carcinoma via suppression of AKT and MAPK signalling

Yang

Velmurugan

Chen

et al. 2022

J Cellular Molecular Medi

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Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer worldwide. Although cisplatin-based chemotherapy is commonly used in HNSCC, frequent development of cisplatin resistance is a potential cause of poor HNSCC prognosis. In the present study, we investigated the anticancer efficacy of a major paclitaxel metabolite namely 7-Epitaxol in cisplatin-resistant HNSCC. The findings revealed that 7-Epitaxol exerts cytotoxic effects in cisplatin-resistant HNSCC cell lines by inducing cell cycle arrest and intrinsic and extrinsic apoptotic pathways. Specifically, 7-Epitaxol increased Fas, TNF-R1, DR5, DcR3 and DcR2 expressions, reduced Bcl-2 and Bcl-XL (anti-apoptotic proteins) expressions, and increased Bid and Bim L/S (pre-apoptotic proteins) expressions, leading to activation of caspase-mediated cancer cell apoptosis.At the upstream cell signalling level, 7-Epitaxol reduced the phosphorylation of AKT, ERK1/2 and p38 to trigger apoptosis. In vivo results showed that animals treated with 7-Epitaxol show antitumor growth compared to control animals. Taken together, the study demonstrates the potential anticancer efficacy of 7-Epitaxol in inducing apoptosis of cisplatin-resistant HNSCC cells through the suppression of AKT and MAPK signalling pathways.

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Section: Discussionsupporting

confidence: 78%

7‐Epitaxol induces apoptosis in cisplatin‐resistant head and neck squamous cell carcinoma via suppression of AKT and MAPK signalling

Yang

Velmurugan

Chen

et al. 2022

J Cellular Molecular Medi

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“…The dual role of p38 MAPK in tumorigeneses was recently described by Martinez-Limon et al, in 2020 [ 49 ], which reflects its anti-tumorigenic activity related to cell cycle arrest, apoptosis and preventing cell proliferation and its tumor-promoting role, characterized by tumor cell migration, resistance to apoptotic stress, chemotherapeutic drugs [ 50 ] and DNA damage repair. In addition, if p38 was inhibited, resistant HNSCC cells showed a higher DNA damage response [ 51 ] and exhibited a decreased expression of cancer stem-cell markers such as CD44 and KLF4 [ 51 , 52 ].…”

Section: Discussionmentioning

confidence: 99%

Interplay between Partial EMT and Cisplatin Resistance as the Drivers for Recurrence in HNSCC

Ingruber

Dudás

Sprung³

et al. 2022

Biomedicines

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This study aims to investigate the role of partial epithelial to mesenchymal transition (pEMT)-related proteins in modulating Cisplatin resistance in head and neck squamous cell carcinoma (HNSCC). SCC-25 cells were pre-treated with TGF-beta1 followed by transient Krüppel-like Factor 4 (KLF4)-overexpression and Cisplatin treatment. Cell growth, cell morphological changes and cell migration were assessed using Juli BR live cell video-microscopy. In addition, Ki-67 and Slug immunostaining and follow-up image cytometric analysis of primary and recurrent HNSCC tumors were performed to evaluate the proliferation index (PI) and the EMT-like phenotype. We observed that proliferating and Slug-positive tumor cells expand after therapy in HNSCC. Subsequently, protein analysis revealed the stabilization of Slug, upregulation of Vimentin and phospho-p38 (p-p38) in Cisplatin-resistant SCC-25 cells. Moreover, KLF4-overexpression contributed to Cisplatin sensitivity by reduction of Slug at the protein level. This work strongly suggests that an pEMT-like pathway is activated in recurrent and Cisplatin-resistant HNSCC. Finally, stable KLF4-overexpression might sensitize HNSCC tumor cells for Cisplatin treatment.

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“…The knockdown of miR 136-5p showed negative regulation of ROCK 1 levels with the suppression of AKT/mTOR pathway that elevated chemoresistance which was reversed with a ROCK 1 molecular inhibitor [ 192 ]. Protein 38, an integral component of the mitogen-activated protein kinase (MAPK) pathway has attenuated cisplatin resistance in HNSCC by interfering with the DNA repair mechanisms [ 193 ]. It has also activated the Wnt/beta – catenin signalling and the expression of cancer stem cell markers in HNSCC resistant to cisplatin therapy [ 193 ].…”

Section: Recent Advances In Cisplatin-associated Head and Neck Cancermentioning

confidence: 99%

“…Protein 38, an integral component of the mitogen-activated protein kinase (MAPK) pathway has attenuated cisplatin resistance in HNSCC by interfering with the DNA repair mechanisms [ 193 ]. It has also activated the Wnt/beta – catenin signalling and the expression of cancer stem cell markers in HNSCC resistant to cisplatin therapy [ 193 ].…”

Section: Recent Advances In Cisplatin-associated Head and Neck Cancermentioning

confidence: 99%

Cisplatin for cancer therapy and overcoming chemoresistance

Ranasinghe

Mathai

Zulli

2022

Heliyon

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p38 Mitogen-activated protein kinase modulates cisplatin resistance in Head and Neck Squamous Cell Carcinoma cells

Cited by 12 publications

References 27 publications

7‐Epitaxol induces apoptosis in cisplatin‐resistant head and neck squamous cell carcinoma via suppression of AKT and MAPK signalling

7‐Epitaxol induces apoptosis in cisplatin‐resistant head and neck squamous cell carcinoma via suppression of AKT and MAPK signalling

Interplay between Partial EMT and Cisplatin Resistance as the Drivers for Recurrence in HNSCC

Cisplatin for cancer therapy and overcoming chemoresistance

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