Reciprocal Regulation of Annexin A2 and EGFR with Her-2 in Her-2 Negative and Herceptin-Resistant Breast Cancer

Shetty, Praveenkumar; Thamake, Sanjay; Biswas, Swati; Johansson, Sonny L.; Vishwanatha, Jamboor K.

doi:10.1371/journal.pone.0044299

Cited by 61 publications

(96 citation statements)

References 57 publications

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“…EGFR plays a role in regulating ANXA2 phosphorylation and localization (30,31). By coimmunoprecipitation assay, we found that p37 interacted with both ANXA2 and EGFR (Fig.…”

Section: Egfr Facilitates M Hyorhinis Infectionmentioning

confidence: 76%

Mycoplasma Hyorhinis Infection Promotes NF-κB–Dependent Migration of Gastric Cancer Cells

Duan

Chen

et al. 2014

Cancer Research

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Chronic infection of Mycoplasma hyorhinis (M. hyorhinis) has been postulated to be associated with several types of cancer, but its effect on patients' survival and host factors mediating its infection remain unclear. Herein, we demonstrated that M. hyorhinis p37 protein expression in gastric cancer tissues predicts poor survival and associates with metastasis. M. hyorhinis infects mammalian cells and promotes gastric cancer cell invasiveness via its membrane protein p37. Synthesized peptide corresponding to the N-terminus of p37 prevents M. hyorhinis infection. Host Annexin A2 (ANXA2) interacts with the N-terminus of p37. In addition, EGFR forms a complex with p37 and ANXA2, and is required for M. hyorhinis-induced phosphorylation and membrane recruitment of ANXA2. M. hyorhinis infection is inhibited by siRNA-mediated knockdown of ANXA2 or EGFR, but is enhanced by expression of ectopic ANXA2 or EGFR. Downstream of ANXA2 and EGFR, the NF-kB pathway is activated and mediates M. hyorhinis-driven cell migration. In conclusion, our study unveils the effect of M. hyorhinis infection on gastric cancer survival and uncovers the mechanisms by which M. hyorhinis infects mammalian cells and promotes cancer cell migration. Cancer Res; 74(20); 5782-94. Ó2014 AACR.

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“…EGFR plays a role in regulating ANXA2 phosphorylation and localization (30,31). By coimmunoprecipitation assay, we found that p37 interacted with both ANXA2 and EGFR (Fig.…”

Section: Egfr Facilitates M Hyorhinis Infectionmentioning

confidence: 76%

Mycoplasma Hyorhinis Infection Promotes NF-κB–Dependent Migration of Gastric Cancer Cells

Duan

Chen

et al. 2014

Cancer Research

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“…We found that M. hyorhinis upregulated Tyr23 phosphorylation of ANXA2 and its membrane recruitment. It was reported that EGFR plays a role in regulating ANXA2 phosphorylation and localization [16] . Moreover, our previous work reported that both M. hyorhinis infection and recombinant p37 treatment could activate EGFR [5,12] , but the role of EGFR in M. hyorhinis infection and M. hyorhinis-induced metastasis are not fully elucidated.…”

Section: Identification Of the Microbial And Host Factors Mediating Mmentioning

confidence: 99%

Mycoplasma hyorhinis: a potential risk factor in gastric cancer progression

Duan

Shou

2015

Can Cell Microenviron

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Persistent infection of Mycoplasma hyorhinis (M. hyorhinis)is associated with various types of cancer. However, the molecule mechanism of M. hyorhinis infection and its effect on cancer patients' prognosis were unknown. Recently, we reported for the first time that M. hyorhinis infects mammalian cells via the interaction of its membrane protein p37 and the host protein Annexin A2 (ANXA2). And NF-B pathway, a downstream of ANXA2, is activated and mediates M. hyorhinis-driven cell migration. Furthermore, we demonstrated that M. hyorhinis p37 protein expression in gastric cancer tissues positively correlates with tumor metastasis and predicts poor survival. In conclusion, our study uncovers the mechanism by which M. hyorhinis infects mammalian cells and promotes cancer cell migration and unveils the effect of M. hyorhinis infection on gastric cancer survival.

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“…There are presently documented eight cofactors for HPV 16 entry into epithelial cells that contribute to selective mucotropism. These include: (1) clathrin coated vesicles, (2) endocytosis, (3) transport protein particle subunit 8, (4) a negative charge molecular display on entry membrane, (5) annexin A2 expression, (6) integrinsα 6 β 14 expression, (7) cyclophillin B activity and (8) growth factor receptors activation, such as EGFR, and tetraspanins [18][19][20][43][44][45]. In addition entry event studies for HPV 16 in HOK are sadly lacking.…”

Section: Experimental Design To Evaluate Oral Commensal Streptococcusmentioning

confidence: 99%

“…proliferation following low level (e.g., 5%,v/v, 50 mg/mL.) ETOH treatment will increase expression of Annexin A2, and EGFR to also enhance HPV 16 entry [13,14,[18][19][20][21][22][23][24][25][26][27][28][29][30][31][32].…”

Section: Set Of Comparative Assays To Examine Associations Of S Salimentioning

confidence: 99%

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Alcohol Treatment of Oral Streptococcus Spp. Increased the Entry of Human Papillomavirus Type 16 into Non-Malignant and Oral Squamous Cell Carcinoma Cells

2014

J Oral Biol

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Background: Oropharyngeal carcinoma is often associated with human papilloma virus subtype 16 (HPV) infections; however events that lead to HPV entry and carcinoma are poorly understood. We simulated a clinical situation in the laboratory by examining human epithelial and oral keratinocyte (HOK) responses to oral commensal bacteria (Streptococcus spp.) and metabolism of ethyl alcohol (ETOH). These studies led us to conclude that oral bacteria and ethyl alcohol through keratinocyte membrane signals act as co-factors for HPV 16 entry. Methods:We tested ETOH exposure responses of Streptococcus spp., ETOH-sensitive, acetaldehyde (AA) producers: S. mutans (LT11), S. salivarius strain, 109-2 and S. gordonii (V2016; wild type). In comparison to ETOH-resistant, non-producers of AA: S. salivarius strain, 101-7 or S. gordonii (adh ABE mutant). 5×105 per cfu/mL of bacteria were exposed to ETOH (5%,v/v) for 1h and then co-incubated for 3h with epithelial targets: immortalized: 293TT; HPV 16 (HOK/HPV 16B cells), or telomerase: hTERT HOK. Streptococci spp. attachment to epithelial cells and subsequent effects were enumerated with immune cytochemistry; Western immunoblotting, and immunoprecipitation techniques. These methods delineated expressions of syndecans-1, 4; phospho-L-tyrosine epidermal growth factor receptor (EGFR), and furin convertase (FC) with HPV 16 pseudo virus (PsV) entry into 293TT, hTERT HOKs and oral squamous cell carcinoma (SCC-25). To verify these relationships we used inhibitors of alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), and FC.Results: Streptococcus spp. metabolism of ETOH released AA to trigger HOK expressions of syndecans 1 and 4 and heparin sulfate binding proteins were degraded by heparanase. Following these events enhanced phosphorylated EGFR expression and HPV 16 entry through FC activity were recorded.Conclusions: Some oral Streptococcus spp. response to ETOH mediates epithelial cell susceptibility to HPV 16 entry. This occurs through membrane associated expression changes of proteoglycans and EGFR. Moreover, oral cancer cell differentiation and growth may be dependent upon these associations.

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Reciprocal Regulation of Annexin A2 and EGFR with Her-2 in Her-2 Negative and Herceptin-Resistant Breast Cancer

Cited by 61 publications

References 57 publications

Mycoplasma Hyorhinis Infection Promotes NF-κB–Dependent Migration of Gastric Cancer Cells

Mycoplasma Hyorhinis Infection Promotes NF-κB–Dependent Migration of Gastric Cancer Cells

Mycoplasma hyorhinis: a potential risk factor in gastric cancer progression

Alcohol Treatment of Oral Streptococcus Spp. Increased the Entry of Human Papillomavirus Type 16 into Non-Malignant and Oral Squamous Cell Carcinoma Cells

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