Krüppel‐like factor 4 induces apoptosis and inhibits tumorigenic progression in SK‐BR‐3 breast cancer cells

Wang, Bing; Zhao, Mingzhi; Cui, Naipeng; Lin, Dandan; Zhang, An-yi; Qin, Yan; Liu, Caiyun; Yan, Weitao; Shi, Jian‐hong; Chen, Baoping

doi:10.1016/j.fob.2015.02.003

Cited by 41 publications

(36 citation statements)

References 37 publications

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“…TNF␣ is a potent inducer of apoptosis in many tumor cell lines (22,23). Consistently, we found that TNF␣ treatment induced apoptosis in BT549 cells, as judged by induction of the apoptotic marker cleaved caspase-3 (Fig.…”

Section: Tnf␣/ap-1 Signaling Regulates Apoptosis and Cell Invasion Ansupporting

confidence: 83%

AP-1 Is a Key Regulator of Proinflammatory Cytokine TNFα-mediated Triple-negative Breast Cancer Progression

Qiao

Jonsson

et al. 2016

Journal of Biological Chemistry

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Section: Tnf␣/ap-1 Signaling Regulates Apoptosis and Cell Invasion Ansupporting

confidence: 83%

AP-1 Is a Key Regulator of Proinflammatory Cytokine TNFα-mediated Triple-negative Breast Cancer Progression

Qiao

Jonsson

et al. 2016

Journal of Biological Chemistry

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“…KLF4 is expressed in various tissues, including epithelial cells, vascular smooth muscle cells and monocytes/macrophages (32,33), but its expression is commonly downregulated in several types of malignant tumor (18,24,34,35). Notably, KLF4 expression is upregulated in breast cancer (36). In the present study, it was identified that KLF4 expression was downregulated in prostate cancer tissues, which was consistent with previous observations (24,37).…”

Section: Discussionsupporting

confidence: 93%

Downregulated Kr�ppel‑like factor�4 expression is associated with the aggressiveness of prostate cancer

Zhang

et al. 2019

Oncol Rep

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Krüppel-like factor 4 (KLF4) is a transcription factor and putative tumor suppressor. However, little is known about its role in the progression of prostate cancer. The aim of the present study was to examine the expression and potential role of KLF4 in prostate cancer. KLF4 and E-cadherin expression in 60 prostate cancer tissues and 60 benign prostatic hyperplasia tissues was characterized by immunohistochemistry. The levels of KLF4 expression in prostate cancer cells were determined by reverse transcription-quantitative polymerase chain reaction and western blot analysis. LNCaP cells were transduced with lentivirus to induce KLF4 overexpression. The effects of KLF4 overexpression on proliferation, cell cycle and migration were determined by MTT, flow cytometry, wound healing and Transwell migration assays. KLF4 was identified to be primarily expressed in the cytoplasm of non-tumor prostate tissues. The percentage of KLF4 + tissues among prostate cancer tissues (16.67%) was significantly lower compared with that of non-tumor tissues (84.67%; P<0.05). Downregulated KLF4 expression was associated with higher stage, positive lymph node metastasis and higher Gleason scores of prostate cancer (all P<0.05). Induction of KLF4 overexpression significantly inhibited the proliferation, wound healing and migration of LNCaP cells and induced their cell cycle arrest at S phase. Furthermore, E-cadherin expression was downregulated in prostate cancer tissues and KLF4 overexpression enhanced the levels of E-cadherin expression in LNCaP cells. In conclusion, downregulated KLF4 expression was associated with aggressiveness of prostate cancer, and KLF4 overexpression inhibited the proliferation, wound healing and migration of prostate cancer cells by inducing cell cycle arrest and E-cadherin expression.

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“…Gefitinib can induce apoptosis by activating the caspase cascade in NSCLC cells carrying the sensitive mutation of EGFR . Krüppel‐like factor 4 also has an ambiguous apoptosis‐induced effect in bladder cancer cells, breast cancer cells, and plasma cells . The present study revealed that knockdown of KLF4 promoted gefitinib‐induced apoptosis by upregulating expression of apoptosis‐related proteins in c‐Met‐overexpressing NSCLC cells (Figure A,C) but not in NSCLC cells without c‐Met overexpression (Figure ), whereas overexpression of KLF4 suppressed gefitinib‐induced apoptosis in gefitinib‐sensitive cells (Figure B,D).…”

Section: Discussionmentioning

confidence: 48%

Krüppel‐like factor 4 promotes c‐Met amplification‐mediated gefitinib resistance in non‐small‐cell lung cancer

et al. 2018

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Gefitinib has been widely used in the first‐line treatment of advanced EGFR‐mutated non‐small‐cell lung cancer (NSCLC). However, many NSCLC patients will acquire resistance to gefitinib after 9‐14 months of treatment. This study revealed that Krüppel‐like factor 4 (KLF4) contributes to the formation of gefitinib resistance in c‐Met‐overexpressing NSCLC cells. We observed that KLF4 was overexpressed in c‐Met‐overexpressing NSCLC cells and tissues. Knockdown of KLF4 increased tumorigenic properties in gefitinib‐resistant NSCLC cell lines without c‐Met overexpression, but it reduced tumorigenic properties and increased gefitinib sensitivity in gefitinib‐resistant NSCLC cells with c‐Met overexpression, whereas overexpression of KLF4 reduced gefitinib sensitivity in gefitinib‐sensitive NSCLC cells. Furthermore, Western blot analysis revealed that KLF4 contributed to the formation of gefitinib resistance in c‐Met‐overexpressing NSCLC cells by inhibiting the expression of apoptosis‐related proteins under gefitinib treatment and activating the c‐Met/Akt signaling pathway by decreasing the inhibition of β‐catenin on phosphorylation of c‐Met to prevent blockade by gefitinib. In summary, this study's results suggest that KLF4 is a promising candidate molecular target for both prevention and therapy of NSCLC with c‐Met overexpression.

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Krüppel‐like factor 4 induces apoptosis and inhibits tumorigenic progression in SK‐BR‐3 breast cancer cells

Cited by 41 publications

References 37 publications

AP-1 Is a Key Regulator of Proinflammatory Cytokine TNFα-mediated Triple-negative Breast Cancer Progression

AP-1 Is a Key Regulator of Proinflammatory Cytokine TNFα-mediated Triple-negative Breast Cancer Progression

Downregulated Kr�ppel‑like factor�4 expression is associated with the aggressiveness of prostate cancer

Krüppel‐like factor 4 promotes c‐Met amplification‐mediated gefitinib resistance in non‐small‐cell lung cancer

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