Curcumin induces apoptosis in p53-null Hep3B cells through a TAp73/DNp73-dependent pathway

Wang, Jinhong; Xie, Honglan; Gao, Feng; Zhao, Tingkun; Yang, Hong-Ming; Kang, Bai

doi:10.1007/s13277-015-4029-3

Cited by 12 publications

(12 citation statements)

References 58 publications

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“…Our data showed that TAp73 and Elk-1 were highly upregulated after rubone monotherapy or PTX and rubone combination therapy (Figure 3F and G). This discrepancy may be explained by the extremely low expression of TAp73 (37) and Elk-1 (38) in Hep3B cells compared to PC3-TXR cells, which means that all known miR-34a regulation pathways are blocked in Hep3B cells. Thus, we conclude that rubone might work as a miR-34a modulator for prostate cancer in a p53 independent manner.…”

Section: Discussionmentioning

confidence: 99%

Micellar Delivery of miR-34a Modulator Rubone and Paclitaxel in Resistant Prostate Cancer

et al. 2017

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Treatment of prostate cancer with paclitaxel (PTX) often fails due to development of chemoresistance caused by downregulation of the tumor suppressor gene miR-34a. In this study, we demonstrate that co-delivery of PTX and 2′-hydroxy-2,4,4′,5,6′-pentamethoxychalcone (termed rubone) drives upregulation of miR-34a and chemosensitizes PTX-resistant prostate cancer cells, killing both cancer stem-like cells (CSCs) and bulk tumor cells. Rubone upregulated miR-34a and reversed its downstream target genes in DU145-TXR and PC3-TXR cells. PTX and rubone combination therapy inhibited tumor cell growth, migration, and CSC population growth. We synthesized poly(ethylene glycol)-block-poly(2-methyl-2-carboxyl-propylene carbonate-graft-dodecanol) (PEG-PCD) to prepare micelles. The drug-loading capacities were 9.70 ± 0.10% and 5.34 ± 0.02% for PTX and rubone, respectively, controlling a drug release of 60.20 ± 2.67% and 60.62 ± 4.35% release of PTX and rubone at 24 h. Delivery of miR-34a and rubone decreased PC3-TXR cell viability with increasing PTX concentration. Co-incubation with a miR-34a inhibitor diminished the effect of rubone. PTX IC50 in PC3 and PC3-TXR cells was 55.6 and 2580 nM, respectively, but decreased to 49.8 and 93.2 nM when treated in combination with rubone, demonstrating a reversal of PTX resistance by rubone. Systemic administration of micelles carrying PTX and rubone inhibited orthotopic prostate tumor growth in nude mice, compared to monotherapy, by reversing the expression of miR-34a, SIRT1, Cyclin D1 and E-cadherin. In summary, our results showed how rubone acts as an efficient small molecule modulator of miR-34a to reverse chemoresistance and further enhance the therapeutic efficacy of PTX in PTX-resistant prostate cancer.

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Section: Discussionmentioning

confidence: 99%

Micellar Delivery of miR-34a Modulator Rubone and Paclitaxel in Resistant Prostate Cancer

et al. 2017

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“…TP53 may induce apoptosis extrinsic or intrinsic pathway triggered via cellular stresses from nutrient deprivation and hypoxia, DNA damage, proliferation and cell survival [293,294]. Curcumin, a yellow pigment of diarylheptanoid isolated from rhizome of Curcuma longa has been extensively studied on its apoptosis inducing capabilities on various cancer cell lines involving p53 modulation [295,296,297]. p53 upon activation, triggered the mitochondria apoptotic pathway by acting as transcription factor that regulates the expression of pro-apoptotic Bcl-2 family member mainly Bax, BH3,phorbol-12-myristate-13-acetate-induced protein 1 (NOXA), and PUMA, and down-regulates the anti-apoptotic Bcl-2, Bcl-xL, and inhibitors of apoptosis proteins (IAPs), which includes Survivin [298].…”

Section: Molecules Target and Signaling Pathway Of Apoptosis Inducmentioning

confidence: 99%

Mechanism of Apoptosis Induced by Curcumin in Colorectal Cancer

Ismail

Othman

Abas

et al. 2019

IJMS

123

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Colorectal cancer (CRC) is among the top three cancer with higher incident and mortality rate worldwide. It is estimated that about over than 1.1 million of death and 2.2 million new cases by the year 2030. The current treatment modalities with the usage of chemo drugs such as FOLFOX and FOLFIRI, surgery and radiotherapy, which are usually accompanied with major side effects, are rarely cured along with poor survival rate and at higher recurrence outcome. This trigger the needs of exploring new natural compounds with anti-cancer properties which possess fewer side effects. Curcumin, a common spice used in ancient medicine was found to induce apoptosis by targeting various molecules and signaling pathways involved in CRC. Disruption of the homeostatic balance between cell proliferation and apoptosis could be one of the promoting factors in colorectal cancer progression. In this review, we describe the current knowledge of apoptosis regulation by curcumin in CRC with regard to molecular targets and associated signaling pathways.

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“…So, the repression of p21 after KCTD11 knock-down in Huh7 could be a result of up-regulated MST1/GSK3β. To further confirm this mechanism, we estimated the changes of Hippo pathway and p21 signaling in the p53-deficient Hep3B cells [28]. Hep3B was treated by siRNA of KCTD11.…”

Section: Resultsmentioning

confidence: 99%

KCTD11 inhibits growth and metastasis of hepatocellular carcinoma through activating Hippo signaling

et al. 2017

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A lack of effective prognostic biomarkers and molecular targets is a serious problem in hepatocellular carcinoma. KCTD11, reported as a tumor suppressor, are still not well understood. In this study, KCTD11 was found low-expressed in HCC tissues and cell lines. The HCC patients with low expression of KCTD11 suggested shorter overall survival. We found KCTD11 inhibiting cell proliferation in vitro and tumor growth in vivo, by activating p21 and repressing cycle related proteins. KCTD11 also inhibited cell adhesion by decreasing CTGF and CLDN1. We found CTGF binding COL3A1 in HCCLM3, which might lead to reduction of COL3A1 expression. KCTD11 also inhibited cell migration and invasion in HCC, by repressing MMPs and EMT. We found the tumor suppression function of KCTD11 was at least partly through activating Hippo pathway in HCC. Base on the enhanced Hippo pathway, KCTD11 could activate p21 by stabilizing p53 or promoting the MST1/ GSK3β/p21 signaling in HCC. Overall, these results suggest that KCTD11 works as a tumor suppressor and owns prognostic and therapeutic potentials in HCC.

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Curcumin induces apoptosis in p53-null Hep3B cells through a TAp73/DNp73-dependent pathway

Cited by 12 publications

References 58 publications

Micellar Delivery of miR-34a Modulator Rubone and Paclitaxel in Resistant Prostate Cancer

Micellar Delivery of miR-34a Modulator Rubone and Paclitaxel in Resistant Prostate Cancer

Mechanism of Apoptosis Induced by Curcumin in Colorectal Cancer

KCTD11 inhibits growth and metastasis of hepatocellular carcinoma through activating Hippo signaling

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