Sohlh2 inhibits breast cancer cell proliferation by suppressing Wnt/β‐catenin signaling pathway

Zhang, Xiaoli; Liu, Ruihua; Zhao, Na; Ji, Shaolin; Hao, Chunyan; Cui, Weiwei; Zhang, Ruihong; Hao, Jing

doi:10.1002/mc.22989

Cited by 17 publications

(12 citation statements)

References 35 publications

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“…Then, 2 independent diagnosticians calculated the semi-quantitative immunoreactivity score (IRS), according to a staining intensity scale: No staining, 0; weak staining, 1; moderate staining, 2; and strong staining, 3; and the number of stained cells: 0, 0; 1-25, 1; 26-50, 2; 51-75, 3; and 76-100%, 4. The final IRS ranged from 0 to 12, and was determined by multiplying the intensity scores with the percent of positively stained cells, as described previously (25).…”

Section: Immunohistochemistry (Ihc)mentioning

confidence: 99%

Effects of cisplatin on the proliferation, invasion and apoptosis of breast cancer cells following β‑catenin silencing

Zhu

Feng

et al. 2020

Int J Mol Med

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Resistance to the chemotherapeutic drug cisplatin has been documented in various types of cancer, while the increased expression of β-catenin has been observed in cisplatin-resistant ovarian cancer. However, the involvement of β-catenin in cisplatin resistance is unclear. The present study investigated the antitumor effect of cisplatin on the proliferation, invasion and apoptosis of breast cancer (Bc) cells following β-catenin silencing in Bc, which is the most frequent type of malignancy among women. The expression of β-catenin in Bc tissues and cell lines was measured by reverse transcription-quantitative polymerase chain reaction, and the association between expression levels and clinical characteristics was statistically analyzed. The viability of Bc cell lines treated with siR-β-catenin or with siR-β-catenin and cisplatin in combination was determined using a cell counting Kit-8 assay. The migratory and invasive abilities of Bc cells treated with both siR-β-catenin and cisplatin were examined with Transwell assays. The cd44 antigen/intercellular adhesion molecule 1 expression ratio, cell cycle distribution and apoptosis levels of Bc cells treated with siR-β-catenin and cisplatin in combination were detected by flow cytometry. The expression levels of apoptosis-associated proteins, including caspase-3/9, in the Bc cells treated with both siR-β-catenin and cisplatin were investigated by western blot analysis. The levels of apoptosis in the Bc cells following combined treatment with siR-β-catenin and cisplatin was further quantified by Hoechst 33342 staining. β-catenin was identified to be highly expressed in Bc tissues and cell lines and was associated with pathological stage and lymph node status. Following knockdown of β-catenin expression, cisplatin treatment suppressed the viabilities, and the migratory and invasive capabilities of the T47d and McF-7 cells, and induced extensive apoptosis. β-catenin knockdown upregulated caspase-3/9 levels following cisplatin treatment and induced the apoptosis of T47d and McF-7 cells. In conclusion, β-catenin may be of value as a therapeutic target during cisplatin treatment in patients with Bc treated with cisplatin.

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Section: Immunohistochemistry (Ihc)mentioning

confidence: 99%

Effects of cisplatin on the proliferation, invasion and apoptosis of breast cancer cells following β‑catenin silencing

Zhu

Feng

et al. 2020

Int J Mol Med

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“…Li et al showed that TRIM63, a novel oncogene, promotes BC cell proliferation and migration via activating the Wnt/ β -catenin signaling pathway [ 34 ]. Also, the silencing of SOHLH2 enhances BC cell proliferation by activating the Wnt/ β -catenin signaling pathway [ 35 ]. Given that SOX4 could stimulate β -catenin activity [ 36 – 38 ], we surmised that circ-DONSON could activate the Wnt/ β -catenin signaling via SOX4.…”

Section: Discussionmentioning

confidence: 99%

Circ-DONSON Knockdown Inhibits Cell Proliferation and Radioresistance of Breast Cancer Cells via Regulating SOX4

Zhu

2021

Journal of Oncology

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Background. Circular RNAs have been validated as critical regulators in the development of breast cancer (BC). Circ-DONSON is involved in the progression of glioma and gastric cancer. However, the biological role of circ-DONSON in BC remains unclear, and the aim of this study was to explore the biological role of circ-DONSON in BC. Methods. Human tissue samples and BC cell lines were collected in this study. siRNAs against circ-DONSON were transfected into BC cell lines for silencing of circ-DONSON. Quantitative real-time PCR was used to test the circ-DONSON expression. Cell counting kit-8 (CCK-8), 5-bromo-2′ deoxyuridine enzyme-linked immunosorbent assay (BrdU-ELISA), colony formation, and caspase-3 activity assays were used to assess cell proliferation, cell survival, and cell viability. Western blotting analysis was used to detect the protein expression levels. Results. Our findings showed that circ-DONSON showed high expression in BC tissues and cell lines. CCK-8 and BrdU-ELISA assays showed that circ-DONSON knockdown inhibited BC cell proliferation. Moreover, cell survival, cell viability, and caspase-3 activity assays showed that circ-DONSON knockdown reduced the radioresistance of BC cells. Mechanistically, circ-DONSON regulated BC cell proliferation and radioresistance via SRY-box transcription factor 4 (SOX4). SOX4 overexpression significantly rescued the effect of circ-DONSON knockdown on BC cell proliferation and radioresistance. Moreover, circ-DONSON activated the Wnt/β-catenin pathway in BC cells via SOX4. Conclusion. Our study concluded that circ-DONSON knockdown hindered cell proliferation and radioresistance through the SOX4/Wnt/β-catenin pathway in BC.

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“…On the other hands, SOHLH2 silence increased migration and invasion, suggesting that this protein may negatively regulate metastasis and play an important role in EMT (Ji et al, 2016). Primary breast tumors express reduced levels of SOHLH2 in comparison with normal tissue (Zhang et al, 2019). Also, SOHLH2 expression is associated to cellular proliferation in vitro and tumor growth in vivo acting as a tumor suppressor gene.…”

Section: Breast Cancermentioning

confidence: 99%

“…Also, SOHLH2 expression is associated to cellular proliferation in vitro and tumor growth in vivo acting as a tumor suppressor gene. The tumor suppressor effects on breast cancer seem to occur due to SOHLH2 inhibition of WNT/β-catenin through the increase of APC (Zhang et al, 2019) (figure 2). Previous data from our group have shown the association between SOHLH2 and triple negative breast cancer (TNBC).…”

Section: Breast Cancermentioning

confidence: 99%

SOHLH2 (spermatogenesis and oogenesis specific basic helix-loop-helix 2)

Mangone¹,

Pavanelli²,

Nagai³

2020

Atlas of Genetics and Cytogenetics in Oncology and Haematology

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Sohlh2 inhibits breast cancer cell proliferation by suppressing Wnt/β‐catenin signaling pathway

Cited by 17 publications

References 35 publications

Effects of cisplatin on the proliferation, invasion and apoptosis of breast cancer cells following β‑catenin silencing

Effects of cisplatin on the proliferation, invasion and apoptosis of breast cancer cells following β‑catenin silencing

Circ-DONSON Knockdown Inhibits Cell Proliferation and Radioresistance of Breast Cancer Cells via Regulating SOX4

SOHLH2 (spermatogenesis and oogenesis specific basic helix-loop-helix 2)

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