Urban Air Rights as Market Devices: Exploring Financialization in Taipei Metropolitan Area

This thesis is the first geographical study which critically explores the role of urban air rights - the right to build upwards on and above a land tract – in processes of urban financialization. The thesis highlights the economic lives of air rights in the Taipei Metropolitan Area, Taiwan, showing how they are not only a market-based urban policy and planning tool but are also closely involved in economic processes of making markets, assets, and profits. Three types of urban air rights - Bonus Floor Area (BFA), Transferable Development Rights (TDR) and Incremental Floor Area (IFA) – that are prevalent in urban Taipei are explored in detail. The thesis examines the relations between the proliferation of air rights production and urban financialization through an experimental methodology of ‘following urban air rights’ through the socio-technical operations of their assembly and circulation. It argues that air rights are ‘market devices’ and, as such, they are constitutive of the contingent processes of commodification, marketization and capitalization that amount to urban financialization. Through case studies, the thesis shows how airspaces are commodified and, significantly, how they also become an asset class that is marketized and traded and/or capitalized upon and borrowed against (i.e. leveraged). Moreover, by exploring these processes, the thesis shows how air rights ‘overflow’ into popular urban politics: air rights become a site of struggle over rights to the financialized city. More broadly, the thesis contributes to theoretical debates on urban financialization by examining how the urban-finance nexus is teeming with socio-technical practices. By focusing on air rights as market devices, the thesis provides an analytical grammar for studying how urban air rights constitute urban financialization. It also demonstrates how a methodology of ‘following the air rights’ enables exploration of the multifaceted qualities and multiple markets that air rights configure

Regulation of RUNX3 in gastric and breast cancer

RUNX3 is a transcription factor that is ubiquitously expressed in different tissues and has been shown to have diverse functions in many developmental procedures. Recently it has also been acknowledged that RUNX3 is involved as a tumor suppressor in many distinct cancers in different tissues. In this thesis, we will examine the regulation of this tumor suppressor in gastric cancer and breast cancer. Chronic infection with cagA-positive Helicobacter pylori is the strongest risk factor for the development of gastric adenocarcinoma. The cagA gene product CagA is injected into gastric epithelial cells and disturbs cellular functions by physically interacting with and deregulating a variety of cellular signaling molecules. RUNX3 is expressed gastric epithelial tissues, and is frequently inactivated in gastric cancer. In the first part of the thesis, we showed that H. pylori infection inactivates the gastric tumor suppressor RUNX3 in a CagA-dependent manner. CagA directly associates with RUNX3 through a specific recognition of the PY motif of RUNX3 by a WW domain of CagA. Deletion of the WW domains of CagA or mutation of the PY motif in RUNX3 abolishes the ability of CagA to induce the ubiquitination and degradation of RUNX3, thereby extinguishing its ability to inhibit the transcriptional activation of RUNX3. This study identify RUNX3 as a novel cellular target of H. pylori CagA and also reveal a mechanism by which CagA functions as an oncoprotein by blocking the activity of gastric tumor suppressor RUNX3. RUNX3 has also been known to be inactivated in breast cancer through dual mechanism of cytoplasmic mislocalization as well as promoter hypermethylation. Recent studies in our lab have shown that RUNX3 knockout mice have an approximate 20% increased chance of ii developing breast cancer compared to WT mice. At the same time, MCF7 cells expressing RUNX3 resulted in smaller tumor growth in a tumorigenicity assay compared to MCF7 cells expressing a control vector, further affirming RUNX3’s importance as a tumor suppressor in breast cancer. Pin1 is an isomerase that is over-expressed in human breast cancer. Pin1 specifically isomerizes only the Ser/Thr-Pro bonds in certain proteins, which allows it to act as a molecular switch controlling protein functions. In the second part of this thesis, we discuss the findings that Pin1 interacts specifically with tumor suppressor protein RUNX3 through 4 separate phosphorylated Ser/Thr-Pro motifs on the RUNX3 protein. Through this interaction with Pin1, the ubiquitination of RUNX3 is markedly enhanced, resulting in decreased protein stability. RUNX3 is therefore targeted to the 26S proteasome for degradation in the presence of Pin1. Our data shows a novel pathway through which tumor suppressor protein RUNX3 can be inactivated and hence regulated in breast tissues by Pin1