HPIP promotes epithelial-mesenchymal transition and cisplatin resistance in ovarian cancer cells through PI3K/AKT pathway activation

Bugide, Suresh; Gonugunta, Vijay K.; Penugurti, Vasudevarao; Malisetty, Vijaya Lakshmi; Vadlamudi, Ratna K.; Manavathi, Bramanandam

doi:10.1007/s13402-016-0308-2

Cited by 52 publications

(38 citation statements)

References 56 publications

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“…The PI3K/AKT pathway is a potential target for therapeutic intervention due to its pivotal role in the regulation of proliferation, survival, and invasiveness of OC [23]. Hematopoietic PBX-interacting protein promoted the migration, invasion, and EMT in OAW42 cells via activation of the PI3K/AKT pathway by directly interacting with PI3K [24]. He et al [25] revealed that exendin-4 inhibit cell growth, migration, and invasion and enhanced apoptosis by inhibiting the PI3K/AKT pathway during OC progression.…”

Section: Discussionmentioning

confidence: 99%

PRR11 Overexpression Facilitates Ovarian Carcinoma Cell Proliferation, Migration, and Invasion Through Activation of the PI3K/AKT/β-Catenin Pathway

Zhu

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Ovarian cancer (OC) is the most lethal gynecologic malignancy, mainly due to the advanced stage at diagnosis in most patients and high rate of relapse. Thus, it is still essential to elucidate the underlying mechanisms and explore the diagnostic and therapeutic targets of OC. Recent studies have revealed that proline-rich protein 11 (PRR11) is dysregulated in different cancers, participating in their initiation and progression; however, it remains unclear whether PRR11 is involved in OC. Methods: Immunohistochemical staining, quantitative reverse transcription PCR, and western blotting were performed to evaluate PRR11 expression in OC tissues and cells. The relationship between PRR11 expression and the clinicopathologic data of patients were analyzed. We upregulated and downregulated PRR11 expression using a PRR11 overexpression vector and PRR11-specifc small interfering RNA, respectively, to further clarify its role in the malignant biological behavior of OC in vitro. Results: Overexpression of PRR11 in OC tissues and cells significantly correlated with advanced FIGO stage, lymph node metastasis, and large tumor size. Downregulation of PRR11 inhibited cell proliferation and prevented the invasion and migration of HO-8910 OC cells, whereas opposite results were observed in Caov3 cells upon PRR11 upregulation. Further analyses showed that PRR11 positively regulated cell proliferation-related proteins, including c-myc and cyclin D1, and increased and decreased the expression of matrix metalloproteinase 2 and tissue inhibitor of metalloproteinase 2, respectively. Additionally, our preliminary results demonstrated that PRR11 expression was mediated by the phosphoinositide 3-kinase/AKT/β-catenin signaling pathway. Conclusion: The results of this study provide evidence that PRR11 plays a critical role in the progression and metastasis of OC, and as such, may serve as a potential prognostic and therapeutic target in OC.

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Section: Discussionmentioning

confidence: 99%

PRR11 Overexpression Facilitates Ovarian Carcinoma Cell Proliferation, Migration, and Invasion Through Activation of the PI3K/AKT/β-Catenin Pathway

Zhu

Wang

et al. 2018

Cell Physiol Biochem

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“…Herein we proposed that NID1 exacerbated resistance of ovarian cancer cells via upregulating the expression of MDR1 and ABCG2 (Figure 8E and Figure 8G), two well-known ABC transporters. Besides NID1, several regulators, such as HPIP, NANOG and FOXM1, have been reported to promote EMT of ovarian cancer cells and then confer them drug resistance, involving PI3K/AKT pathway, STAT3 pathway, etc [33–36]. The aforementioned results implicated that NID1-overexpressed ovarian cancer cells potentially exhibited cancer stem cell-like characteristics which imparts the metastatic and chemoresistant advantage to cells.…”

Section: Discussionmentioning

confidence: 99%

NID1, a new regulator of EMT required for metastasis and chemoresistance of ovarian cancer cells

et al. 2017

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Nidogen-1 (NID1) has been identified as a novel candidate diagnostic biomarker of ovarian cancer in our previous study. Nevertheless, the role of NID1 in the pathogenesis of ovarian cancer is unclear. In the present study, we demonstrated that NID1 was a mesenchymal associated gene and its high expression was significantly correlated with shorter overall survival of ovarian cancer patients. The ectopic expression of NID1 in OVCAR-3 cells revealed a epithelial-mesenchymal transition (EMT) phenotype accompanied by enhancement of motility, invasiveness and cisplatin resistance, whereas the knockdown of NID1 was sufficient to convert HEY cells into epithelial phenotype with decreased capability of motility, invasiveness and cisplatin resistance. Mechanistic studies disclosed that NID1 activated ERK/MAPK signaling pathway to promote EMT. Collectively, our findings have uncovered the molecular mechanisms of NID1 in promoting ovarian cancer metastasis and chemoresistance, and provide a rationale for the therapeutic potential of NID1 suppression in ovarian cancer.

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“…Numerous studies have demonstrated that microRNAs (miRNAs) are involved in the process of epithelial-mesenchymal transition (EMT) in various types of cancer (3)(4)(5)(6), and various studies have revealed that the EMT may be associated with the drug resistance of cancer cells (7)(8)(9)(10). Furthermore, by comparing the miRNA expression profiles between breast cancer cell lines in our previous study, we determined that the expression of miR-93 was increased markedly in drug-resistant MCF-7/AdrVp cells compared with the parental MCF-7 cell line (11).…”

Section: Introductionmentioning

confidence: 99%

miR-93 and PTEN: Key regulators of doxorubicin-resistance and EMT in breast cancer

Chu

Xia

et al. 2017

Oncology Reports

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Abstract. It is not well established whether miR-93 is involved in drug resistance and epithelial-mesenchymal transition (EMT) in breast cancer, and its underlying mechanism remains uncertain. In the present study, the expression differences of miR-93 between paired breast cancer tissues confirmed it is involved in the progression of breast cancer. Such a difference was also observed in doxorubicin-resistant and -sensitive cells. Overexpressed miR-93 in sensitive cells revealed increases in cellular proliferation and the expression levels of drug-resistant-related genes, and a decrease in sensitivity to doxorubicin. This demonstrated the relationship between miR-93 and breast cancer drug resistance. Simultaneously, EMT was confirmed in miR-93 overexpressing sensitive cells. This indicated the triadic relationship among miR-93, EMT and drug resistance in breast cancer. We applied the Dual-luciferase Reporter assay to expose the direct interaction between miR-93 and PTEN, which suggested that miR-93 contributes to inducing EMT and drug resistance of breast cancer cells by targeting PTEN.

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HPIP promotes epithelial-mesenchymal transition and cisplatin resistance in ovarian cancer cells through PI3K/AKT pathway activation

Cited by 52 publications

References 56 publications

PRR11 Overexpression Facilitates Ovarian Carcinoma Cell Proliferation, Migration, and Invasion Through Activation of the PI3K/AKT/β-Catenin Pathway

PRR11 Overexpression Facilitates Ovarian Carcinoma Cell Proliferation, Migration, and Invasion Through Activation of the PI3K/AKT/β-Catenin Pathway

NID1, a new regulator of EMT required for metastasis and chemoresistance of ovarian cancer cells

miR-93 and PTEN: Key regulators of doxorubicin-resistance and EMT in breast cancer

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