Effect of LIV1 on the sensitivity of ovarian cancer cells to trichostatin A

Ma, Xiaoli; Duan, Hua; Liu, Jia; Mo, Qingqing; Sun, Chang; Ma, Ding; Wang, Jiandong

doi:10.3892/or.2014.3622

Cited by 4 publications

(4 citation statements)

References 27 publications

(29 reference statements)

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“…expression was observed in a number of cancers including pancreas (Unno et al, 2009(Unno et al, , 2014, prostate (L. Cao, 2012;Lue et al, 2011;Yamashita et al, 2004), liver (Lian et al, 2016;Shen et al, 2013), melanoma, breast, ovary (Ma et al, 2009(Ma et al, , 2015, cervical (Chen et al, 2019;Lue et al, 2011;Zhao et al, 2007), uterine, esophageal carcinoma (Cheng et al, 2017;Wu et al, 2013), gastric (J. Gao et al, 2019) and lung carcinoma (Sussman et al, 2014;Wan et al, 2018).…”

Section: Genomic Regulation Of Liv1 and Role In Cancermentioning

confidence: 99%

“…In pre‐clinical models, LIV1 expression was found to be associated with epithelial‐to‐mesenchymal transition—in embryonic development, cancer promotion, and progression (GeneMANIA, 2021). LIV1 expression was observed in a number of cancers including pancreas (Unno et al, 2009, 2014), prostate (L. Cao, 2012; Lue et al, 2011; Yamashita et al, 2004), liver (Lian et al, 2016; Shen et al, 2013), melanoma, breast, ovary (Ma et al, 2009, 2015), cervical (Chen et al, 2019; Lue et al, 2011; Zhao et al, 2007), uterine, esophageal carcinoma (Cheng et al, 2017; Wu et al, 2013), gastric (J. Gao et al, 2019) and lung carcinoma (Sussman et al, 2014; Wan et al, 2018).…”

Section: Genomic Regulation Of Liv1 and Role In Cancermentioning

confidence: 99%

See 1 more Smart Citation

Zinc transporter LIV1: A promising cell surface target for triple negative breast cancer

Saravanan

Balasubramanian

Balamurugan

et al. 2022

Journal Cellular Physiology

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Breast cancer is one of the leading causes contributing to the global cancer burden.The triple negative breast cancer (TNBC) molecular subtype accounts for the most aggressive type. Despite progression in therapeutic options and prognosis in breast cancer treatment options, there remains a high rate of distant relapse. With advancements in understanding the role of zinc and zinc carriers in the prognosis and treatment of the disease, the scope of precision treatment/targeted therapy has been expanded. Zinc levels and zinc transporters play a vital role in maintaining cellular homeostasis, tumor surveillance, apoptosis, and immune function. This review focuses on the zinc transporter, LIV1, as an essential target for breast cancer prognosis and emerging treatment options. Previous studies give an insight into the role of LIV1 in fulfilling the most important hallmarks of cancer such as apoptosis, metastasis, invasion, and evading the immune system. Normal tissue expression of LIV1 is limited. Higher expression of LIV1 has been linked to Epithelial-Mesenchymal Transition, histological grade of cancer, and early node metastasis. LIV1 was found to be one of the attractive targets in the therapeutic hunt for TNBCs. TNBCs are an immunogenic breast cancer subtype. As zinc transporters are known to serve as the metabolic gatekeepers of immune cells, this review bridges tumor infiltrating lymphocytes, TNBC and LIV1. In addition, the suitability of LIV1 as an antibody-drug conjugate (Seattle genetics [SGN]-LIV1A) target in TNBC, represents a promising strategy for patients. Early clinical trial results reveal that this novel agent reduces tumor burden by inducing mitotic arrest, immunomodulation, and immunogenic cell death, warranting further investigation of SGN-LIV1A in combination with immunooncology agents. Priming the patient's immune response in combination with SGN-LIV1A could eventually change the landscape for the TNBC patient population.

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Section: Genomic Regulation Of Liv1 and Role In Cancermentioning

confidence: 99%

Section: Genomic Regulation Of Liv1 and Role In Cancermentioning

confidence: 99%

Zinc transporter LIV1: A promising cell surface target for triple negative breast cancer

Saravanan

Balasubramanian

Balamurugan

et al. 2022

Journal Cellular Physiology

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show abstract

“…Thus, TF-fVIIa-dependent inflammatory responses may be enhanced if Zn 2+ levels within EOC tissues are increased. EOC cells can express zinc transporters such as LIV1 [164,165] and hZIP1 [166] to uptake extracellular Zn 2+ , potentially leading to accumulation of Zn 2+ within cells. However, one study reported that Zn 2+ levels within EOC tissues and plasma of EOC patients were lower than those in benign tissues and normal controls, respectively [167].…”

Section: Potential Roles Of Metal Ions In Coagulation Factor-drivementioning

confidence: 99%

Potential Coagulation Factor-Driven Pro-Inflammatory Responses in Ovarian Cancer Tissues Associated with Insufficient O2 and Plasma Supply

Koizume¹,

Miyagi²

2017

IJMS

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Tissue factor (TF) is a cell surface receptor for coagulation factor VII (fVII). The TF-activated fVII (fVIIa) complex is an essential initiator of the extrinsic blood coagulation process. Interactions between cancer cells and immune cells via coagulation factors and adhesion molecules can promote progression of cancer, including epithelial ovarian cancer (EOC). This process is not necessarily advantageous, as tumor tissues generally undergo hypoxia due to aberrant vasculature, followed by reduced access to plasma components such as coagulation factors. However, hypoxia can activate TF expression. Expression of fVII, intercellular adhesion molecule-1 (ICAM-1), and multiple pro-inflammatory cytokines can be synergistically induced in EOC cells in response to hypoxia along with serum deprivation. Thus, pro-inflammatory responses associated with the TF-fVIIa–ICAM-1 interaction are expected within hypoxic tissues. Tumor tissue consists of multiple components such as stromal cells, interstitial fluid, albumin, and other micro-factors such as proton and metal ions. These factors, together with metabolism reprogramming in response to hypoxia and followed by functional modification of TF, may contribute to coagulation factor-driven inflammatory responses in EOC tissues. The aim of this review was to describe potential coagulation factor-driven inflammatory responses in hypoxic EOC tissues. Arguments were extended to clinical issues targeting this characteristic tumor environment.

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“…Previously, the present study investigated whether the HDACi trichostatin A (TSA) induces apoptosis of ovarian cancer A2780 cells in a dose-dependent manner (6). Thus far, numerous HDACis are being tested in over 100 clinical trials and have exhibited encouraging therapeutic responses with good safety profiles (7,8).…”

Section: Introductionmentioning

confidence: 99%

Targeting CD146 in combination with vorinostat for the treatment of ovarian cancer cells

Wang

Liu

et al. 2017

Oncology Letters

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Drug resistance is the predominant cause of mortality in late-stage patients with ovarian cancer. Histone deacetylase inhibitors (HDACis) have emerged as a novel type of second line drug with high specificity for tumor cells, including ovarian cancer cells. However, HDACis usually exhibit relatively low potencies when used as a single agent. The majority of current clinical trials are combination strategies. These strategies are more empirical than mechanism-based applications. Previously, it was reported that the adhesion molecule cluster of differentiation 146 (CD146) is significantly induced in HDACi-treated tumor cells. The present study additionally confirmed that the induction of CD146 is a common phenomenon in vorinostat-treated ovarian cancer cells. AA98, an anti-CD146 monoclonal antibody (mAb), was used to target CD146 function. Synergistic antitumoral effects between AA98 and vorinostat were examined in vitro and in vivo. The potential effect of combined AA98 and vorinostat treatment on the protein kinase B (Akt) pathway was determined by western blotting. The present study found that targeting of CD146 substantially enhanced vorinostat-induced killing via the suppression of activation of Akt pathways in ovarian cancer cells. AA98 in combination with vorinostat significantly inhibited cell proliferation and increased apoptosis. In vivo, AA98 synergized with vorinostat to inhibit tumor growth and prolong survival in ovarian cancer. These data suggest that an undesired induction of CD146 may serve as a protective response to offset the antitumor efficacy of vorinostat. By contrast, targeting CD146 in combination with vorinostat may be exploited as a novel strategy to more effectively kill ovarian cancer cells.

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Effect of LIV1 on the sensitivity of ovarian cancer cells to trichostatin A

Cited by 4 publications

References 27 publications

Zinc transporter LIV1: A promising cell surface target for triple negative breast cancer

Zinc transporter LIV1: A promising cell surface target for triple negative breast cancer

Potential Coagulation Factor-Driven Pro-Inflammatory Responses in Ovarian Cancer Tissues Associated with Insufficient O2 and Plasma Supply

Targeting CD146 in combination with vorinostat for the treatment of ovarian cancer cells

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