Regulation of inflammation and tumorigenesis by the TIPE family of phospholipid transfer proteins

Goldsmith, Jason R.; Chen, Youhai H.

doi:10.1038/cmi.2017.4

Cited by 76 publications

(57 citation statements)

References 79 publications

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“…TNFAIP8 is the principal member of this family that is induced by TNF-α in response to environmental stress (11). It has previously been identified that TNFAIP8 is overexpressed in a wide range of different cancer types, and additional previous studies have demonstrated that it serves as an oncoprotein, as it induces the development and progression of tumors, and enhances cancer cell survival, proliferation and metastasis (12,23,24). However, little is known regarding the biological and pathological functions of TNFAIP8 in cervical cancer.…”

Section: Discussionmentioning

confidence: 99%

“…as an anti-apoptotic and pro-oncogenic signaling molecule (9)(10)(11)(12). A previous study suggested that tumor necrosis factor α (TNF-α) stimulation and the activation of the nuclear factor-κB pathway may upregulate the mRNA expression levels of TNFAIP8 in head and neck squamous cell carcinoma cell lines (13).…”

Section: Tnfaip8 Promotes Cisplatin Resistance In Cervical Carcinoma mentioning

confidence: 99%

“…A previous study suggested that tumor necrosis factor α (TNF-α) stimulation and the activation of the nuclear factor-κB pathway may upregulate the mRNA expression levels of TNFAIP8 in head and neck squamous cell carcinoma cell lines (13). In addition, TNFAIP8 overexpression was associated with cancer progression and poor prognosis in a number of different cancer types (12,(14)(15)(16)(17)(18). Silencing TNFAIP8 in a variety of cells promoted cellular apoptosis, attenuated cellular proliferation and the production of matrix metalloproteinase (MMP)-1 and MMP-9 (19).…”

Section: Tnfaip8 Promotes Cisplatin Resistance In Cervical Carcinoma mentioning

confidence: 99%

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TNFAIP8 promotes cisplatin resistance in cervical carcinoma cells by inhibiting cellular apoptosis

Su-xia

et al. 2019

Oncol Lett

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Cervical cancer is the second most prevalent malignant tumor in women worldwide. Failure of successful treatment is most prevalent in patients with the metastatic disease and the chemotherapy refractory disease. Tumor necrosis factor α-induced protein 8 (TNFAIP8) serves as an anti-apoptotic and pro-oncogenic protein, and is associated with cancer progression and poor prognosis in a number of different cancer types. However, the physiological and pathophysiological roles of TNFAIP8 in cervical carcinogenesis and development remain poorly understood. In the present study, it was demonstrated that TNFAIP8 protein expression levels were significantly increased in cervical cancer tissues compared with the non-tumor adjacent tissues using immunohistochemistry. Additionally, it was demonstrated that TNFAIP8 overexpression is associated with cisplatin resistance. Furthermore, depletion of TNFAIP8 impaired HeLa cell proliferation and viability in vitro, improved cisplatin sensitivity, and promoted cisplatin-induced cellular apoptosis and death. Subsequent mechanistic analysis demonstrated that TNFAIP8 silencing promoted caspase-8/-3 activation and p38 phosphorylation in HeLa cells treated with cisplatin, whereas apoptosis regulator B-cell lymphoma-2 expression was inhibited with TNFAIP8-silenced HeLa cells following treatment with cisplatin. These data suggested that TNFAIP8 serves as an anti-apoptotic protein against cisplatin-induced cell death, which eventually leads to chemotherapeutic drug-treatment failure. Therefore, the present data suggested that TNFAIP8 may be a promising therapeutic target for the treatment of cervical cancer.Abbreviations: TNFAIP8, tumor necrosis factor α-induced protein 8; MAPK, mitogen-activated protein kinase; CDDP, Cis-diamminedichloroplatinum

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Section: Discussionmentioning

confidence: 99%

Section: Tnfaip8 Promotes Cisplatin Resistance In Cervical Carcinoma mentioning

confidence: 99%

Section: Tnfaip8 Promotes Cisplatin Resistance In Cervical Carcinoma mentioning

confidence: 99%

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TNFAIP8 promotes cisplatin resistance in cervical carcinoma cells by inhibiting cellular apoptosis

Su-xia

et al. 2019

Oncol Lett

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“…In the present study, murine macrophage Raw264.7 and T lymphocyte EL4 cells were transfected with Migr1 control and a TIPE overexpression vector due to their abilities for suitable DNA transfection (18). In despite of the fact that TIPE is a newly described regulator of immunity and tumorigenesis and is the only known transfer protein of the lipid second messengers (22,23), the exact mechanism of TIPE-mediated pro-survival effects remain uncertain. In the present study, we observed that TIPE inhibited cell apoptosis and promoted tumor formation in vivo.…”

Section: Discussionmentioning

confidence: 99%

TIPE attenuates the apoptotic effect of radiation and cisplatin and promotes tumor growth via JNK and p38 activation in Raw264.7 and EL4 cells

et al. 2018

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Tumor necrosis factor α‑induced protein 8 (TIPE) is highly expressed in many types of malignancies. Apoptosis is the process of programmed cell death which maintains the balance of cell survival and death. TIPE is involved in the carcinogenesis of many tumor types, yet the exact role of TIPE in defective apoptosis‑associated carcinogenesis remains uncertain. In the present study, TIPE‑overexpressing Raw264.7 and EL4 cells and vector control cells were treated with 4 mJ/cm2 ultraviolet radiation or 2 µg/ml cisplatin. Following ultraviolet irradiation, TIPE overexpression decreased the percentage of apoptotic cells as detected by flow cytometric and reversed the cisplatin‑mediated decrease in mitochondrial membrane potential by JC‑1 assay. Western blot analyses also revealed that TIPE overexpression inhibited cisplatin‑induced activation of caspase‑3 and ‑9 and PARP. Secondly, TIPE overexpression increased the levels of phosphorylated JNK, MEK and p38. Moreover, inhibition of JNK and p38, but not MEK, efficiently abolished the cell pro‑survival effect of TIPE. Most importantly, an in vivo tumor implantation model revealed that TIPE overexpression augmented the volume and weight of the implanted tumors, indicating that TIPE facilitated tumor formation. We found that TIPE exhibited an anti‑apoptotic effect via JNK and p38 activation, which ultimately promoted tumor. Hence, the present study revealed that activation of JNK and p38 kinases contribute to the TIPE‑mediated anti‑apoptotic effect, indicating that JNK and p38 may be potential therapeutic molecules for TIPE overexpression‑associated diseases.

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“…The TIPE (tumor necrosis factor-α induced protein 8) family are newly described regulators of immunity and tumorigenesis and are composed of four highly homologous proteins: TNFAIP8 (TIPE), TNFAIP8L1 (TIPE1), TNFAIP8L2 (TIPE2) and TNFAIP8L3 (TIPE3) [6,7]. TNFAIP8, also known as SCC-S2, GG2-1, NDED, and MDC-3.13, was the first described member of the TIPE family.…”

Section: Ivyspringmentioning

confidence: 99%

TNFAIP8 promotes the migration of clear cell renal cell carcinoma by regulating the EMT

Zhong¹,

Zhu²,

Liu³

et al. 2020

J. Cancer

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Background: Clear cell renal cell carcinoma (ccRCC) is characterized by high metastatic potential, and the epithelial-mesenchymal transition (EMT) has been shown to play a key role in multiple cancer progression, migration and metastasis and is the leading cause of poor prognosis. Currently, tumor necrosis factor-α-induced protein 8 (TNFAIP8/TIPE) is a newly discovered tumorigenesis factor, and TNFAIP8 and the EMT influence the migration of renal cancer cells. Methods: In this study, we first analyzed the relationship between TNFAIP8 and ccRCC using bioinformatics, followed by immunohistochemistry to evaluate the relationship between the two in clinical samples. Subsequently, reverse transcription PCR and western blotting confirmed the expression of TNFAIP8 in ccRCC cells. Furthermore, we measured the migration and invasion abilities by using wound healing and transwell assays after overexpression or knockdown of TNFAIP8 in cells. In addition, we verified whether TNFAIP8 affects the EMT process in ccRCC by quantitative real-time PCR, western blotting, immunohistochemistry and immunofluorescence experiments. Results: Through database analysis, we found that TNFAIP8 was highly expressed in ccRCC patients and was positively correlated with tumor stage and grade, indicating that TNFAIP8 is associated with the development of advanced ccRCC and poor prognosis. We subsequently confirmed that TNFAIP8 was abnormally overexpressed in clinical samples and ccRCC cell lines and that TNFAIP8 promoted ccRCC cell migration and invasion in vitro. Finally, we found that TNFAIP8 regulated EMT-related molecule expression and regulated the EMT process. Conclusion: High expression of TNFAIP8 reinforces migration and regulates the EMT in ccRCC, conferring the metastatic potential of ccRCC and suggesting that TNFAIP8 may be a potential therapeutic target for the treatment of advanced ccRCC.

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Regulation of inflammation and tumorigenesis by the TIPE family of phospholipid transfer proteins

Cited by 76 publications

References 79 publications

TNFAIP8 promotes cisplatin resistance in cervical carcinoma cells by inhibiting cellular apoptosis

TNFAIP8 promotes cisplatin resistance in cervical carcinoma cells by inhibiting cellular apoptosis

TIPE attenuates the apoptotic effect of radiation and cisplatin and promotes tumor growth via JNK and p38 activation in Raw264.7 and EL4 cells

TNFAIP8 promotes the migration of clear cell renal cell carcinoma by regulating the EMT

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