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J Cancer Metastasis Treat 2020;6:5 I http://dx.doi.org/10.20517/2394-4722.2020.13 Page 25 of 38

Results: RNA-seq identified seven differentially expressed tRFs between pre-and postoperative plasmas
in patients with NSCLC. Among them, the expression of a novel tRF termed AS-tDR-007333 was
significantly upregulated in preoperative plasma, NSCLC tissues, and NSCLC cell lines. Overexpression
of AS-tDR-007333 promoted NSCLC cell (PC9, HCC827, and A549) proliferation, while knockdown of
AS-tDR-007333 inhibited cell growth. RNA-seq showed that up-regulation of AS-tDR-007333 led to the
activation of oncogenes such as MED29, AL049829.1, SCHIP1, SAMD12, MRFAP1, and SHISA5. RNA
pulldown and RIP analyses revealed that AS-tDR-007333 can bind directly with heat shock protein beta-1
(HSPB-1). Rescue assays demonstrated that HSPB1 was involved in AS-tDR-007333 mediated NSCLC cell
proliferation.

Conclusion: Our study reveals an oncogenic role of AS-tDR-007333 in NSCLC, suggesting that it may be a
novel target for diagnosis and the treatment of NSCLC.

35. Breast tumor-on-chip

Subia Bano

Elvesys Microfluidics Innovation Centre Paris, Paris 75011, France.

Background and aim: Breast cancer is the most common invasive cancer among women. There are several
chemotherapeutic and radiotherapeutic approaches available but they have certain limitations. Over the
past few years, improved understanding of the microenvironment heterogeneity of breast cancer has
allowed the development of more effective treatment strategies. However, researchers have still not been
able to recapitulate the entire tumor microenvironment to study tumor progression and invasion. In this
way, more complex 3D in vitro cancer models have been developed. These 3D tumor models still lack the
cell-cell and cell-tissue interactions and more balanced interstitial fluidic flow that are present within living
systems. Furthermore, mimicking different physiological conditions and collecting samples from tumor
microenvironment are also difficult. In this direction, the breast tumor-on-chip model has emerged as an
alternative system to study the tumor microenvironment and decipher its role in metastasis. In this work,
a microfluidics system was integrated into a 3D breast tumor to bridge the gap between 2D and animal
model effectively and evaluate the efficacy of anti-cancerous drugs. These microfluidic systems contain
small chambers for cell culture, which enable control over local gradients and the ability to maintain the
interstitial fluidic flow of the local breast tumor microenvironment.

Experimental procedure: In this work, the multi-compartment microfluidics platform was generated by
designing a specific PDMS chip with three channels that are separated by specific barriers (50 µm). The
cancerous and fibroblast cells (cocultures) were suspended with collagen hydrogel and loaded into the
central channel and one of the side channels was used to grow the endothelial cells to make this system
vascularized. The barriers inside the chips allowed exchanging signaling molecules.

Results: The cancer cells in the presence of fibroblast cells grew well in these microchannels, which was
confirmed with live/dead assay. At this stage, we have obtained the preliminary data and are still working in
this area.

Conclusion: Integration of microfluidics system into breast tumor will add another toolset that can make a
more efficient testing platform for the current therapeutic development pipeline.