Suppression of TWIST1 enhances the sensitivity of colon cancer cells to 5-fluorouracil

Sakowicz-Burkiewicz, Monika; Przybyła, Tomasz; Wesserling, Martyna; Bielarczyk, Hanna; Maciejewska, Izabela; Pawełczyk, Tadeusz

doi:10.1016/j.biocel.2016.07.024

Cited by 20 publications

(13 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previously we have reported that suppression TWIST1 enhanced the sensitivity of colon cancer cells to 5FU. [ 17 ] In the present study, the most noticeable effect of TWIST1 suppression on sensitivity of colon cancer cell lines to combined treatment of 5FU and the MAPKs inhibitors was observed for inhibitors of p38α/βand JNK1-3. We also noted that the suppression of TWIST1 significantly sensitized both cell lines to combined treatment of 5FU and Rac inhibitor.…”

Section: Discussionmentioning

confidence: 48%

“…The knockdown of TWIST1 was performed as described previously. [ 17 ] Briefly, the TWIST1 silencing sequence (shRNA) was subcloned into the pLL3.7 lentiviral vector (Addgene, Cambridge, MA, USA). The pLL3.7 vector with scrambled oligo was used as a negative control.…”

Section: Methodsmentioning

confidence: 99%

“…The qualitative assessment of TWIST1 was performed by Western blot as described previously. [ 17 ] Rabbit anti- TWIST1 (Abcam, Cambridge, MA, USA) (2.5 μg/ml), and goat anti-rabbit immunoglobulin G (IgG) alkaline phosphatase conjugate (Sigma-Aldrich, St. Louis, MO, USA) were used as a primary and secondary antibody, respectively. For detection of β-actin (reference), mouse anti-β-actin monoclonal antibody (Sigma-Aldrich, St. Louis, MO, USA) was used.…”

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

The Level of TWIST1 expression determines the response of colon cancer cells to mitogen-activated protein kinases inhibitors

Przybyła¹,

Wesserling²,

Sakowicz-Burkiewicz³

et al. 2018

Saudi J Gastroenterol

Self Cite

View full text Add to dashboard Cite

Background/Aim:Currently, it has been proposed that combination of 5-fluorouracil (5FU) with inhibitors of the mitogen-activated protein kinases (MAPKs) signaling pathway might enhance the efficacy of 5FU-based chemotherapy in colon cancer. Our study aimed to investigate an impact of TWIST1 silencing on the sensitivity of cancer cells to 5FU and selected MAPK inhibitors.Materials and Methods:The suppression of TWIST1 expression in human colon cancer HT29 and HCT116 cell lines was achieved by transduction with lentiviral vector carrying the TWIST1 silencing sequence (pLL3.7-sh TWIST1). The statistical calculation was performed with analysis of variance or Dunnett's test for comparison to control group. Paired Student's t-test was performed when two groups were analyzed.Results:Suppression of TWIST1 reduced the proliferation rate of colon cancer cells and enhanced their sensitivity to 5FU and MAPKs inhibitors. The sensitivity of HT29 cells to examined compounds was more dependent on TWIST1 expression level compared to HCT116 cells. The most noticeable effect of TWIST1 suppression on sensitivity of both colon cancer cell lines to combined treatment of 5FU and the MAPKs inhibitors was observed for inhibitors of p38α/β and JNK1-3. We also noted that the suppression of TWIST1 significantly sensitized both cell lines to combined treatment of 5FU and Rac inhibitor.Conclusions:Our observations point to TWIST1 expression level as a marker of colon cancer sensitivity to combined treatment of 5FU and MAPKs inhibitors.

show abstract

Section: Discussionmentioning

confidence: 48%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

The Level of TWIST1 expression determines the response of colon cancer cells to mitogen-activated protein kinases inhibitors

Przybyła¹,

Wesserling²,

Sakowicz-Burkiewicz³

et al. 2018

Saudi J Gastroenterol

Self Cite

View full text Add to dashboard Cite

show abstract

“…Higher expression of TP, UP and OPRT levels displayed enhanced sensitivity to 5-FU therapy[ 10 - 12 ]. Similarly, as DPD contributes to the degradation of 5-FU, its expression level was inversely correlated with chemosensitivity[ 11 ]. Collectively, inhibition of the activity of these enzymes could allow enhanced sensitivity to 5-FU.…”

Section: Introductionmentioning

confidence: 99%

Drug resistance and new therapies in colorectal cancer

Jeught

et al. 2018

WJG

433

220

View full text Add to dashboard Cite

Colorectal cancer (CRC) is often diagnosed at an advanced stage when tumor cell dissemination has taken place. Chemo- and targeted therapies provide only a limited increase of overall survival for these patients. The major reason for clinical outcome finds its origin in therapy resistance. Escape mechanisms to both chemo- and targeted therapy remain the main culprits. Here, we evaluate major resistant mechanisms and elaborate on potential new therapies. Amongst promising therapies is α-amanitin antibody-drug conjugate targeting hemizygous p53 loss. It becomes clear that a dynamic interaction with the tumor microenvironment exists and that this dictates therapeutic outcome. In addition, CRC displays a limited response to checkpoint inhibitors, as only a minority of patients with microsatellite instable high tumors is susceptible. In this review, we highlight new developments with clinical potentials to augment responses to checkpoint inhibitors.

show abstract

“…Twist1 has been found to be upregulated in a lot of tumors such as gastric cancer, ovarian cancer, breast cancer, bladder cancer and also osteosarcoma [ 52 – 56 ]. Increasing studies suggested that Twist1 was involved in drug resistance of cancer [ 55 , 57 , 58 ]. In our study, we firstly used the TargetScan databases to show that there is a putative binding site of miR-610 and Twist1.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-610 suppresses osteosarcoma oncogenicity via targeting TWIST1 expression

Jin

Feng

et al. 2017

Oncotarget

View full text Add to dashboard Cite

Osteosarcoma is the most frequent primary bone tumor affects adolescents and young adults. Recently, microRNAs (miRNAs) are short, non-coding and endogenous RNAs that played as important roles in the initiation and progression of tumors. In this study, we try to explore the biological function and expression of miR-610 in the osteosarcoma. We showed that miR-610 expression was downregulated in the osteosarcoma tissues and cell lines. Elevated expression of miR-610 suppressed the osteosarcoma cell proliferation, cell cycle, invasion and EMT program. Moreover, overexpression of miR-610 increased sensitivity of MG-63 and U2OS cells to cisplatin. Twist1 was identified as a direct target gene of miR-610 in the osteosarcoma cell. Furthermore, we demonstrated that Twist1 was upregulated in the osteosarcoma tissues and cell lines. The expression of Twist1 was negatively associated with the expression of miR-610 expression in the osteosarcoma tissues. Ectopic expression of Twist1 inhibited the sensitivity of miR-610-overexpressing MG-63 cells to cisplatin. We also showed that overexpression of Twist1 increased the proliferation and invasion of miR-610-overexpressing MG-63 cells. These data indicated that ectopic expression of miR-610 suppressed the osteosarcoma cell proliferation, cell cylce, invasion and increased the sensitivity of osteosarcoma cells to cisplatin through targeting the Twist1 expression.

show abstract

Suppression of TWIST1 enhances the sensitivity of colon cancer cells to 5-fluorouracil

Cited by 20 publications

References 37 publications

The Level of TWIST1 expression determines the response of colon cancer cells to mitogen-activated protein kinases inhibitors

The Level of TWIST1 expression determines the response of colon cancer cells to mitogen-activated protein kinases inhibitors

Drug resistance and new therapies in colorectal cancer

MicroRNA-610 suppresses osteosarcoma oncogenicity via targeting TWIST1 expression

Contact Info

Product

Resources

About