Transcription factor KLF2 enhances the sensitivity of breast cancer cells to cisplatin by suppressing kinase WEE1

Li, Ruiqing; Chen, Jiejing; Gao, Xiaokang; Jiang, Guoqin

doi:10.1080/15384047.2021.1949228

Cited by 8 publications

(3 citation statements)

References 54 publications

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“…In the meantime, targeting WEE1 has been identified as a potential therapeutic strategy for several cancers, including lung, ovarian, and gastric cancer. 18 , 31 , 32 Our results suggest that WEE1 could also be a viable therapeutic target for EAC.…”

Section: Discussionmentioning

confidence: 69%

Smoking induces WEE1 expression to promote docetaxel resistance in esophageal adenocarcinoma

Islam,

Thangaretnam,

et al. 2023

Molecular Therapy - Oncolytics

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Section: Discussionmentioning

confidence: 69%

Smoking induces WEE1 expression to promote docetaxel resistance in esophageal adenocarcinoma

Islam,

Thangaretnam,

et al. 2023

Molecular Therapy - Oncolytics

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“…For example, several transcription factors have been identified as drivers of breast cancer, including ARNT2, COX7RP, EGR3, FOXA1, FOXC2, FOXM1, FOXO3, NR3C2, and ZNF652. These transcription factors are involved in various cellular processes, including cell division, senescence, cell cycle regulation, and immune cell infiltration in breast cancer [4][5][6][7].…”

Section: Introductionmentioning

confidence: 99%

MEF2D Functions as a Tumor Suppressor in Breast Cancer

Wang,

Shen,

Chen

et al. 2024

IJMS

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The myocyte enhancer factor 2 (MEF2) gene family play fundamental roles in the genetic programs that control cell differentiation, morphogenesis, proliferation, and survival in a wide range of cell types. More recently, these genes have also been implicated as drivers of carcinogenesis, by acting as oncogenes or tumor suppressors depending on the biological context. Nonetheless, the molecular programs they regulate and their roles in tumor development and progression remain incompletely understood. The present study evaluated whether the MEF2D transcription factor functions as a tumor suppressor in breast cancer. The knockout of the MEF2D gene in mouse mammary epithelial cells resulted in phenotypic changes characteristic of neoplastic transformation. These changes included enhanced cell proliferation, a loss of contact inhibition, and anchorage-independent growth in soft agar, as well as the capacity for tumor development in mice. Mechanistically, the knockout of MEF2D induced the epithelial-to-mesenchymal transition (EMT) and activated several oncogenic signaling pathways, including AKT, ERK, and Hippo-YAP. Correspondingly, a reduced expression of MEF2D was observed in human triple-negative breast cancer cell lines, and a low MEF2D expression in tissue samples was found to be correlated with a worse overall survival and relapse-free survival in breast cancer patients. MEF2D may, thus, be a putative tumor suppressor, acting through selective gene regulatory programs that have clinical and therapeutic significance.

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“…KLF2 recruited the SP1/CPBP to down regulate the WEE1 that sensitized ovarian tumor cells toward the DNA damage mediated apoptosis [ 77 ]. It has been suggested that KLF2 can be introduced as a promising target to increase the sensitivity of breast cancer (BCa) to cisplatin via down regulation of WEE1 [ 135 ]. KLF2 promoted cell apoptosis while inhibited cell proliferation through p16, p21, and p27 up regulations and CCND1 and survivin down regulations in breast tumor cells [ 136 ].…”

Section: Introductionmentioning

confidence: 99%

PRC2 mediated KLF2 down regulation: a therapeutic and diagnostic axis during tumor progression

Taghehchian,

Maharati,

Akhlaghipour

et al. 2023

Cancer Cell Int

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Surgery and chemo-radiotherapy are used as the common first-line treatment options in many cancers. However, tumor relapse is observed in many cancer patients following such first-line treatments. Therefore, targeted therapy according to the molecular cancer biology can be very important in reducing tumor recurrence. In this regard, a wide range of monoclonal antibodies against the growth factors and their receptors can offer more targeted treatment in cancer patients. However, due to the importance of growth factors in the normal biology of body cells, side effects can also be observed following the application of growth factor inhibitors. Therefore, more specific factors should be introduced as therapeutic targets with less side effects. Krüppel-like factors 2 (KLF2) belongs to the KLF family of transcription factors that are involved in the regulation of many cellular processes. KLF2 deregulations have been also reported during the progression of many tumors. In the present review we discussed the molecular mechanisms of KLF2 during tumor growth and invasion. It has been shown that the KLF2 as a tumor suppressor is mainly inhibited by the non-coding RNAs (ncRNAs) through the polycomb repressive complex 2 (PRC2) recruitment. This review is an effective step towards introducing the KLF2 as a suitable diagnostic and therapeutic target in cancer patients.

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Transcription factor KLF2 enhances the sensitivity of breast cancer cells to cisplatin by suppressing kinase WEE1

Cited by 8 publications

References 54 publications

Smoking induces WEE1 expression to promote docetaxel resistance in esophageal adenocarcinoma

Smoking induces WEE1 expression to promote docetaxel resistance in esophageal adenocarcinoma

MEF2D Functions as a Tumor Suppressor in Breast Cancer

PRC2 mediated KLF2 down regulation: a therapeutic and diagnostic axis during tumor progression

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