Trefoil factor 3 (TFF3) enhances the oncogenic characteristics of prostate carcinoma cells and reduces sensitivity to ionising radiation

Perera, Omesha N.; Evans, Angharad; Pertziger, Mikhail; Macdonald, Courtney; Chen, Helen; Liu, Dong-Xu; Lobie, Peter E.; Perry, Jo K.

doi:10.1016/j.canlet.2015.02.051

Cited by 31 publications

(42 citation statements)

References 21 publications

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“…This is consistent with our previous studies demonstrating that TFF3 stimulates cell proliferation, survival, migration, and 3D and anchorage-independent cell growth of mammary and prostate carcinoma cells [16, 17, 20, 21]. Literature evidence also suggests a clinical correlation of TFF3 with HCC.…”

Section: Discussionsupporting

confidence: 93%

“…Recent studies have reported that TFF3 expression is increased during the development and progression of human cancers, including gastric [15], breast [16, 17], colon [18], and prostate carcinomas [19] among others. TFF3 has previously been shown to stimulate survival and proliferation of mammary and prostatic carcinoma cells [16, 20]. In addition, we have previously demonstrated that TFF3 promotes metastasis and angiogenesis in mammary carcinoma [17, 21].…”

Section: Introductionmentioning

confidence: 99%

“…Importantly, increasing evidence has also supported a crucial role of TFF3 in decreasing therapeutic sensitivity and mediating therapeutic resistance. For example, our recent study has revealed that TFF3 reduces the sensitivity of prostate carcinoma cells to ionizing radiation [20]. Furthermore, several studies have also implicated functional involvement of TFF3 in resistance towards tamoxifen and aromatase inhibitors in mammary carcinomas [16, 22].…”

Section: Introductionmentioning

confidence: 99%

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Trefoil factor 3 mediation of oncogenicity and chemoresistance in hepatocellular carcinoma is AKT-BCL-2 dependent

et al. 2017

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The efficacious treatment of hepatocellular carcinoma (HCC) remains a challenge, partially being attributed to intrinsic chemoresistance. Previous reports have observed increased TFF3 expression in HCC. Herein, we investigated the functional role of TFF3 in progression of HCC, and in both intrinsic and acquired chemoresistance. TFF3 expression was observed to be upregulated in HCC and associated with poor clinicopathological features and worse patient survival outcome. Functionally, forced expression of TFF3 in HCC cell lines increased cell proliferation, cell survival, anchorage-independent and 3D matrigel growth, cell invasion and migration, and in vivo tumor growth. In contrast, depleted expression of TFF3 decreased the oncogenicity of HCC cells as indicated by the above parameters. Furthermore, forced expression of TFF3 decreased doxorubicin sensitivity of HCC cells, which was attributed to increased doxorubicin efflux and cancer stem cell-like behavior of Hep3B cells. In contrast, depletion of TFF3 increased doxorubicin sensitivity and decreased cancer stem cell-like behavior of Hep3B cells. Correspondingly, TFF3 expression was markedly increased in Hep3B cells with acquired doxorubicin resistance, while the depletion of TFF3 resulted in re-sensitization of the Hep3B cells to doxorubicin. The increased doxorubicin efflux and enhanced cancer stem cell-like behavior of the doxorubicin-resistant Hep3B cells was observed to be dependent on TFF3 expression. In addition, we determined that TFF3-stimulated oncogenicity and chemoresistance in HCC cells was mediated by AKT-dependent expression of BCL-2. Hence, therapeutic inhibition of TFF3 should be considered to hinder HCC progression and overcome intrinsic and acquired chemoresistance in HCC.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Trefoil factor 3 mediation of oncogenicity and chemoresistance in hepatocellular carcinoma is AKT-BCL-2 dependent

et al. 2017

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“…Overexpression of TFF3 was caused changes in mRNA levels associated with the cellular proliferation, apoptosis, migration, invasion and clonogenic survival. Forced expression of TFF3 decreased mRNA expression of BAX, TIMP2, CDKN2A, SERPINB5 and CDH1, but increased mRNA levels of CDH2, VIM, TGFB1, TERT, SERPINE1, TWIST, KI67, SURVIVIN, MMP2 and MMP3 which closely correlated with increasing cell cycle progression, anti-apoptosis, proliferation, metastasis and invasion of cervical cancer cells [9, 10, 28, 29]. …”

Section: Discussionmentioning

confidence: 99%

“…Upregulation of TFF3 after rectal cancer chemo-radiotherapy is an adverse prognostic factor [9]. Furthermore, in prostate carcinoma cells, TFF3 reduces the sensitivity to ionizing-radiation [10]. …”

Section: Introductionmentioning

confidence: 99%

Overexpression of trefoil factor 3 (TFF3) contributes to the malignant progression in cervical cancer cells

Zhang

Chen

et al. 2017

Cancer Cell Int

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BackgroundThere remains a great need for effective therapies for cervical cancers, the majority of which are aggressive leaving patients with poor prognosis.Methods and resultsHere, we identify a novel candidate therapeutic target, trefoil factor 3 (TFF3) which overexpressed in cervical cancer cells and was associated with reduced postoperative survival. Functional studies demonstrated that TFF3 overexpression promoted the proliferation and invasion of cervical cancer cells, and inhibited the apoptosis by inducing the mRNA changes in SiHa and Hela cell lines. Conversely, TFF3 silencing disrupted the proliferation and invasion of cervical cancer cells, and induced the apoptosis via Click-iT EdU test, flow cytometry analysis and two-dimensional Matrigel Transwell analysis. Western blot analysis showed that overexpression of TFF3 repressed E-cadherin (CDH1) expression to promote the invasion of cervical cancer cells. Furthermore, down-regulated CDH1 via overexpression of TFF3 was significantly up-regulated by virtue of inhibitor of p-STAT3.ConclusionsThese results suggested that TFF3 stimulated the invasion of cervical cancer cells probably by activating the STAT3/CDH1 signaling pathway. Furthermore, overexpression of TFF3 decreased the sensitivity of cervical cancer cells to etoposide by increasing P-glycoprotein (P-gp) functional activity. Overall, our work provides a preclinical proof that TFF3 not only contributes to the malignant progression of cervical cancers and but also is a potential therapeutic target.Electronic supplementary materialThe online version of this article (doi:10.1186/s12935-016-0379-1) contains supplementary material, which is available to authorized users.

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Landscape of NcRNAs involved in drug resistance of breast cancer

Kang

2023

Clin Transl Oncol

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Breast cancer (BC) leads to the most amounts of deaths among women. Chemo-, endocrine-, and targeted therapies are the mainstay drug treatments for BC in the clinic. However, drug resistance is a major obstacle for BC patients, and it leads to poor prognosis. Accumulating evidences suggested that noncoding RNAs (ncRNAs) are intricately linked to a wide range of pathological processes, including drug resistance. Till date, the correlation between drug resistance and ncRNAs is not completely understood in BC. Herein, we comprehensively summarized a dysregulated ncRNAs landscape that promotes or inhibits drug resistance in chemo-, endocrine-, and targeted BC therapies. Our review will pave way for the effective management of drug resistance by targeting oncogenic ncRNAs, which, in turn will promote drug sensitivity of BC in the future.

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Trefoil factor 3 (TFF3) enhances the oncogenic characteristics of prostate carcinoma cells and reduces sensitivity to ionising radiation

Cited by 31 publications

References 21 publications

Trefoil factor 3 mediation of oncogenicity and chemoresistance in hepatocellular carcinoma is AKT-BCL-2 dependent

Trefoil factor 3 mediation of oncogenicity and chemoresistance in hepatocellular carcinoma is AKT-BCL-2 dependent

Overexpression of trefoil factor 3 (TFF3) contributes to the malignant progression in cervical cancer cells

Landscape of NcRNAs involved in drug resistance of breast cancer

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