Role of Oct4–Sox2 complex decoy oligodeoxynucleotides strategy on reverse epithelial to mesenchymal transition (EMT) induction in HT29-ShE encompassing enriched cancer stem-like cells

Bigdelou, Zahra; Mortazavi, Yousef; Saltanatpour, Zohreh; Asadi, Zoleykha; Kadivar, Mehdi; Johari, Behrooz

doi:10.1007/s11033-020-05280-2

Cited by 25 publications

(14 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, a role for Sox2 in the growth of SCC was recently reported 47 . Sox2 is known to suppress the expression of E‐cadherin and ZO‐1 and to enhance the expression of multiple EMT‐related genes 48,49 . Thus, reduction in Sox2 may represent an important mechanism driven by OVOL1 upregulation in Twist1 KO mice that contributes to the effects observed on keratinocyte behavior.…”

Section: Discussionmentioning

confidence: 95%

Twist1 is required for the development of UVB‐induced squamous cell carcinoma

Eguiarte-Solomon

Blazanin

Rho

et al. 2021

Molecular Carcinogenesis

View full text Add to dashboard Cite

The transcription factor Twist1 has been reported to be essential for the formation and invasiveness of chemically induced tumors in mouse skin. However, the impact of keratinocyte‐specific Twist1 deletion on skin carcinogenesis caused by UVB radiation has not been reported. Deletion of Twist1 in basal keratinocytes of mouse epidermis using K5.Cre × Twist1flox/flox mice led to significantly reduced UVB‐induced epidermal hyperproliferation. In addition, keratinocyte‐specific deletion of Twist1 significantly suppressed UVB‐induced skin carcinogenesis. Further analyses revealed that deletion of Twist1 in cultured keratinocytes or mouse epidermis in vivo led to keratinocyte differentiation. In this regard, deletion of Twist1 in epidermal keratinocytes showed significant induction of early and late differentiation markers, including TG1, K1, OVOL1, loricrin, and filaggrin. Similar results were obtained with topical application of harmine, a Harmala alkaloid that leads to degradation of Twist1. In contrast, overexpression of Twist1 in cultured keratinocytes suppressed calcium‐induced differentiation. Further analyses using both K5.Cre × Twist1flox/flox mice and an inducible system where Twist1 was deleted in bulge region keratinocytes showed loss of expression of hair follicle stem/progenitor markers, including CD34, Lrig1, Lgr5, and Lgr6. These data support the conclusion that Twist1 has a direct role in maintaining the balance between proliferation and differentiation of keratinocytes and keratinocyte stem/progenitor populations. Collectively, these results demonstrate a critical role for Twist1 early in the process of UVB skin carcinogenesis, and that Twist1 may be a novel target for the prevention of cutaneous squamous cell carcinoma.

show abstract

Section: Discussionmentioning

confidence: 95%

Twist1 is required for the development of UVB‐induced squamous cell carcinoma

Eguiarte-Solomon

Blazanin

Rho

et al. 2021

Molecular Carcinogenesis

View full text Add to dashboard Cite

show abstract

“…The migration and invasion assays were established, as previously described by Bigdelou et al (2020) and Rahmati, Johari et al (2020). Briefly, transfected cells with decoy ODNs, SCR ODNs, and Lipofectamine (test and controls, respectively) were exposed to X‐rays (2 Gy; FD) and MTX (20 nM) and cultured overnight.…”

Section: Methodsmentioning

confidence: 99%

Evaluation of STAT3 decoy oligodeoxynucleotides' synergistic effects on radiation and/or chemotherapy in metastatic breast cancer cell line

Johari

Rahmati

Nasehi

et al. 2020

Cell Biology International

Self Cite

View full text Add to dashboard Cite

Resistance to radiotherapy and chemotherapy has been a major problem of conventional cancer therapies, which consequently leads to cancer relapse and cancer‐related death. It is known that cancer stem cells (CSCs) play a key role in therapy resistance and CSC‐based targeted therapies have been considered as a powerful tool for cancer treatment. In the current study, we investigated the synergistic effects of suppressing signal transducer and activator of transcription (STAT3) function by decoy ODNs on X‐irradiation (XI) and methotrexate (MTX) exposure as a combinational therapy in triple‐negative breast cancer (TNBC) MDA‐MB‐231 cells. Lipofectamine 2000® was used as a transfecting agent and the cells treated with Scramble ODNs (SCR) and decoy ODNs were subjected to irradiation with 2 Gy at single/fractionated (XI group) doses, different concentration of MTX group, and X‐irradiation‐methotrexate (XI/MTX group). Synergistic effects of STAT3 SCR and decoy ODNs on cells were investigated by cell viability (MTT), cell cycle profile, apoptosis rate, migration, and invasion assays. Statistical analysis of obtained data showed that STAT3 decoy ODNs significantly decreased the cell viability, arrested the growth at G0/G1 phase, increased apoptosis rate, and reduced migrated and invaded cells through transwell membrane, in XI, MTX, and XI/MTX exposed groups. Since STAT3 is a master transcription factor in breast cancer cells stemness, aggressiveness, TNBC's heterogeneity, and therapy resistance; therefore, inhibition of this transcription factor by decoy ODNs could increase antitumor efficiencies of XI and MTX exposure strategies. Accordingly, this method could have the potential to increase the efficiency of combination therapies.

show abstract

“…And they bind to specific target genes to induce their expression and jointly maintain CSC-like characteristics. However, whether the OCT4/SOX2 complex works may be related to post-translational modification and the specific mechanism is not clear (5,7,9). Subsequently, it was discovered that OCT4/Lys-156 has different post-translational modifications in human pluripotent stem cells and differentiated cells, which may affect the stability of the OCT4/SOX2 complex and regulate the EMT phenotype (73).…”

Section: Oct4/sox2 Protein Complexmentioning

confidence: 99%

“…Octamer-binding transcription factor 4 (OCT4), which is encoded by the Pou5f1 gene and is a member of the POU-domain transcription factor family, is connected to maintain pluripotency of embryonic stem cells (ESCs) and CSCs (5)(6)(7). Mouse Oct4 has two homologs, Oct4A and Oct4B, the former in the nucleus and the latter in the cytoplasm (8).…”

Section: Introductionmentioning

confidence: 99%

The Role and Specific Mechanism of OCT4 in Cancer Stem Cells: A Review

Zhang

Han

Zhu

et al. 2020

IJSC

View full text Add to dashboard Cite

Recently, evidences show that cancer stem cells (CSCs) are a type of cancer cell group with self-renewal and play a huge role in tumor recurrence, metastasis, and drug resistance. Finding new treatment directions and targets for cancer prognosis and reducing mortality has become a top priority. OCT4, as a transcription factor, participates in maintaining the stem characteristics of CSCs, but the mechanism of OCT4 is often overlooked. In this review, we try to illustrate the mechanism by which OCT4 plays a role in CSCs from the perspective of genetic modification of OCT4, non-coding RNA, complexes and signaling pathways associated with OCT4. Our ultimate goal is to provide new targets for cancer treatment to prolong the survival of cancer patients.

show abstract

Role of Oct4–Sox2 complex decoy oligodeoxynucleotides strategy on reverse epithelial to mesenchymal transition (EMT) induction in HT29-ShE encompassing enriched cancer stem-like cells

Cited by 25 publications

References 49 publications

Twist1 is required for the development of UVB‐induced squamous cell carcinoma

Twist1 is required for the development of UVB‐induced squamous cell carcinoma

Evaluation of STAT3 decoy oligodeoxynucleotides' synergistic effects on radiation and/or chemotherapy in metastatic breast cancer cell line

The Role and Specific Mechanism of OCT4 in Cancer Stem Cells: A Review

Contact Info

Product

Resources

About