High TBX2 expression predicts poor prognosis in non-small cell lung cancer

Zhang, Z; Guo, Yongjun

doi:10.4149/neo_2014_059

Cited by 14 publications

(12 citation statements)

References 11 publications

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“…TBX2 may serve as a prognostic factor of breast cancer (7,9), melanoma (8), gastric cancer (10), prostate cancer (11), laryngeal squamous cell carcinoma (12), and non-small cell lung cancer (14). TBX2 is associated with resistance to therapeutic drugs such as cisplatin and doxorubicin (15,16), and TBX2 therefore may serve as a therapeutic target.…”

Section: Discussionmentioning

confidence: 99%

“…TBX2 is overexpressed by numerous human cancers (7)(8)(9)(10)(11)(12)(13)(14). TBX2 may serve as a prognostic factor of breast cancer (7,9), melanoma (8), gastric cancer (10), prostate cancer (11), laryngeal squamous cell carcinoma (12), and non-small cell lung cancer (14).…”

Section: Discussionmentioning

confidence: 99%

“…TBX2 allows cells to bypass senescence through its ability to repress the activities of the cell cycle regulators p21 and p14 ARF , and silencing TBX2 expression induces senescence (5)(6)(7)(8). Overexpression of TBX2 occurs in breast cancer (7,9), melanoma (8) pancreatic cancer (10), gastric cancer (11), prostate cancer (12), laryngeal squamous cell carcinoma (13), and non-small cell lung cancer (14). The ectopic expression of TBX2 is associated with resistance to the DNA-damaging chemotherapeutic drugs cisplatin and doxorubicin (15,16).…”

Section: Introductionmentioning

confidence: 99%

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TBX2 expression is associated with platinum‑sensitivity of ovarian serous carcinoma

et al. 2017

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Abstract. The standard treatment for ovarian serous carcinoma comprises maximum debulking surgery and platinum-based chemotherapy. Despite the high response rate to chemotherapy, the majority of patients will be resistant to first-line agents and the prognosis for these patients is particularly poor. At present there are no reliable methods to determine or predict platinum resistance. T-box 2 (TBX2) is widely expressed in cancer cells and is involved in embryonic development and cell cycle regulation. TBX2 enables cells to bypass senescence through its ability to repress the cell cycle regulators p21 and p14 ARF ; silencing TBX2 induces senescence. Ectopic expression of TBX2 is associated with conferred resistance to the DNA-damaging chemotherapeutic drugs cisplatin and doxorubicin. In the present study the association between TBX2 expression and platinum sensitivity was investigated. A total of 54 patients with ovarian serous carcinoma (FIGO stages III and IV) were treated at Osaka City University Hospital (Osaka, Japan) from January 2005 to December 2012. Patients were divided into platinum-sensitive (n=27) and resistant (n=27) groups, according to the platinum-free interval calculated from the last platinum administration to the time of recurrence. TBX2 expression in human ovarian serous carcinoma cells was inhibited by a TBX2-specific siRNA and changes in cisplatin and carboplatin sensitivity were determined. The TBX2-weighted score was significantly lower in the platinum-sensitive group than the platinum-resistant group (P=0.005) and the low TBX2 expression group was significantly more sensitive to platinum-based chemotherapy (P=0.004). Sensitivity to cisplatin and carboplatin significantly increased when TBX2 expression was inhibited in human ovarian serous carcinoma cells in vitro (P<0.05). TBX2 expression may serve as a predictive marker of the efficacy of platinum-based chemotherapy for patients with ovarian serous carcinoma.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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TBX2 expression is associated with platinum‑sensitivity of ovarian serous carcinoma

et al. 2017

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“…Earlier reports have suggested that expression levels of TBX2 are elevated in NSCLC [ 39 , 40 ]. The reports by Hu et al [ 39 ] and Zhang et al [ 40 ] interrogated TBX2 protein by immunohistochemistry in NSCLCs alone (tissue microarrays) and suggested that tumors with relatively high expression of the protein (based on percent positivity within the tumors themselves) exhibited comparatively poor prognosis [ 39 , 40 ]. The same reports studied expression levels of the TBX2 gene (e.g.…”

Section: Discussionmentioning

confidence: 99%

“…The same reports studied expression levels of the TBX2 gene (e.g. by quantitative real-time PCR) in NSCLCs and paired normal lung tissues in a smaller subset of NSCLC cases ( n = 40 to 50) [ 39 , 40 ] demonstrating that the gene is elevated in the tumors. These earlier studies [ 39 – 41 ], albeit few, point to putative oncogenic roles and properties for the TBX2 gene in human NSCLC.…”

Section: Discussionmentioning

confidence: 99%

TBX2subfamily suppression in lung cancer pathogenesis: a high-potential marker for early detection

et al. 2017

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The TBX2 subfamily (TBXs 2, 3, 4 and 5) transactivates or represses genes involved in lung organogenesis. Yet TBX2 subfamily expression in pathogenesis of non-small cell lung cancer (NSCLC), the most common lung malignancy, remains elusive. We sought to probe the expression profile of the TBX2 subfamily in early phases of NSCLC. Expression of TBX2 subfamily was analyzed in datasets of pan-normal specimens as well as NSCLCs and normal lung tissues. TBX2 subfamily expression in matched normal lungs, premalignant hyperplasias and NSCLCs was profiled by transcriptome sequencing. TBX2 subfamily expression was evaluated in the cancerization field consisting of matched NSCLCs and adjacent cytologically-normal airways relative to distant normal lungs and in a dataset of normal bronchial samples from smokers with indeterminate nodules suspicious for malignancy. Statistical analysis was performed using R. TBX2 subfamily expression was markedly elevated in normal lungs relative to other organ-specific normal tissues. Expression of the TBXs was significantly suppressed in NSCLCs relative to normal lungs (P < 10−9). TBX2 subfamily was significantly progressively decreased across premalignant lesions and NSCLCs relative to normal lungs (P < 10−4). The subfamily was significantly suppressed in NSCLCs and adjacent normal-appearing airways relative to distant normal lung tissues (P < 10−15). Further, suppressed TBX2 subfamily expression in normal bronchi was associated with lung cancer status (P < 10−5) in smokers. Our findings suggest that the TBX2 subfamily is notably suppressed in human NSCLC pathogenesis and may serve as a high-potential biomarker for early lung cancer detection in high-risk smokers.

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Role of T‐box genes in cancer, epithelial‐mesenchymal transition, and cancer stem cells

Niu

Hao

Sui

et al. 2021

J of Cellular Biochemistry

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Sharing a common DNA binding motif called T-box, transcription factor T-box gene family controls embryonic development and is also involved in cancer progression and metastasis. Cancer metastasis shows therapy resistance and involves complex processes. Among them, epithelial-mesenchymal transition (EMT) triggers cancer cell invasiveness and the acquisition of stemness of cancer cells, called cancer stem cells (CSCs). CSCs are a small fraction of tumor bulk and are capable of self-renewal and tumorsphere formation. Recent progress has highlighted the critical roles of T-box genes in cancer progression, EMT, and CSC function, and such regulatory functions of T-box genes have emerged as potential therapeutic candidates for cancer. Herein we summarize the current understanding of the regulatory mechanisms of T-box genes in cancer, EMT, and CSCs, and discuss the implications of targeting T-box genes as anticancer therapeutics.

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High TBX2 expression predicts poor prognosis in non-small cell lung cancer

Cited by 14 publications

References 11 publications

TBX2 expression is associated with platinum‑sensitivity of ovarian serous carcinoma

TBX2 expression is associated with platinum‑sensitivity of ovarian serous carcinoma

TBX2subfamily suppression in lung cancer pathogenesis: a high-potential marker for early detection

Role of T‐box genes in cancer, epithelial‐mesenchymal transition, and cancer stem cells

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