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The mechanical role of the glycocalyx in cancer cell adhesion

Award Number: K00CA245789
ORGANIZATION: NATIONAL CANCER INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 09/16/2020
PERIOD OF PERFORMANCE END DATE: 11/30/2024

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The mechanical role of the glycocalyx in cancer cell adhesion - Project Summary Many types of cancer – such as recurrent glioblastoma multiform, which is invariably lethal – overexpress bulky glycoproteins to form a thick glycocalyx layer. The glycocalyx physically separates the cell from its surroundings, but recent work has shown that the glycocalyx can paradoxically increase adhesion to soft tissues and therefore promote the metastasis of cancer cells. This surprising phenomenon occurs because the glycocalyx forces adhesion molecules (called integrins) on the cell's surface into clusters. These integrin clusters have cooperative effects that allow them to form stronger adhesions to surrounding tissues than would be possible with equivalent numbers of un-clustered integrins. These cooperative mechanisms have been intensely scrutinized in recent years; a more nuanced understanding of the biophysical underpinnings of glycocalyx- mediated adhesion could uncover therapeutic targets, deepen our general understanding of cancer metastasis, and elucidate general biophysical processes that extend far beyond the realm of cancer research. Here I present the hypothesis that the glycocalyx has the additional effect of increasing mechanical tension experienced by clustered integrins. Integrins function as mechanosensors that undergo structure-switching into “active” conformations when subjected to mechanical tension. As such, my hypothesis would, if true, suggest a more immediate regulatory role of the glycocalyx in adhesion than previously realized. This hypothesis (which I call the local organization hypothesis) is well-supported through indirect observation in the research literature but has not been directly tested due to challenges associated with measuring mechanical tension on individual biomolecules in live cells. However, I have devoted much of my career to developing DNA-based mechanosensor tools that can be used to directly measure piconewton-scale integrin tension in live cells. Here I propose to utilize these tools to test the local organization hypothesis and bring clarity to this rapidly-growing research field. I plan to image integrin forces during the early stages of cellular adhesion and test for a set of specific observations that would support or refute the local organization hypothesis. In parallel, I plan to leverage my computational skills to test this hypothesis using a sophisticated chemomechanical simulation method. For my postdoctoral (K00) work, I will transition into translational work and develop tools that leverage the principles of glycocalyx-mediated adhesion for cancer diagnostic purposes. Because glycocalyx-presenting cancer cells adhere more readily to soft substrates, I will develop a flow-based method for detecting circulating tumor cells (CTCs) using soft substrates and substrates of varying stiffness that facilitate mechanoselection of glycocalyx-presenting cancer cells. This mechanoselection-based method will enable mechanical profiling of CTCs to determine what types of tissues are most vulnerable to metastasis and will also allow for conventional biochemical profiling in parallel. This work will deliver a substantially enhanced understanding of the mechanisms of metastasis, as well as tools that can put this improved understanding to diagnostic use in clinical settings.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2025 ( Subtotal = -$5,147 )
2025	2024	DUKE UNIVERSITY	2200 W MAIN ST	DURHAM	NC	27705	DURHAM	USA	Cancer Cause and Prevention Research	000	5	3/26/2025	NON-COMPETING CONTINUATION	-$5,147
														Subtotal = -$5,147

Issue Date FY: 2024 ( Subtotal = $96,143 )
2024	2024	DUKE UNIVERSITY	2200 W MAIN ST	DURHAM	NC	27705	DURHAM	USA	Cancer Cause and Prevention Research	000	5	11/24/2023	NON-COMPETING CONTINUATION	$96,143
														Subtotal = $96,143

Issue Date FY: 2023 ( Subtotal = $91,837 )
2023	2023	DUKE UNIVERSITY	2200 W MAIN ST	DURHAM	NC	27705	DURHAM	USA	Cancer Cause and Prevention Research	000	4	5/3/2023	NON-COMPETING CONTINUATION	$91,837
														Subtotal = $91,837

Issue Date FY: 2022 ( Subtotal = $87,577 )
2022	2022	DUKE UNIVERSITY	2200 W MAIN ST	DURHAM	NC	27705	DURHAM	USA	Cancer Cause and Prevention Research	003	3	3/28/2022	CHANGE OF GRANTEE / TRAINING INSTITUTION / AWARDING INSTITUTION	$12,281
2022	2022	DUKE UNIVERSITY	2200 W MAIN ST STE 710	DURHAM	NC	27708	DURHAM	USA	Cancer Cause and Prevention Research	001	3	3/14/2022	CHANGE OF GRANTEE / TRAINING INSTITUTION / AWARDING INSTITUTION	$87,577
2022	2020	REGENTS OF THE UNIVERSITY OF MICHIGAN	503 THOMPSON ST	ANN ARBOR	MI	48109	WASHTENAW	USA	Cancer Cause and Prevention Research	000	2	3/14/2022	EXTENSION WITH OR WITHOUT FUNDS	$0
2022	2020	REGENTS OF THE UNIVERSITY OF MICHIGAN	503 THOMPSON STREET	ANN ARBOR	MI	48109	WASHTENAW	USA	Cancer Cause and Prevention Research	002	2	3/28/2022	EXTENSION WITH OR WITHOUT FUNDS	-$12,281
														Subtotal = $87,577

Issue Date FY: 2020 ( Subtotal = $93,600 )
2020	2020	REGENTS OF THE UNIVERSITY OF MICHIGAN	503 THOMPSON ST	ANN ARBOR	MI	48109	WASHTENAW	USA	Cancer Cause and Prevention Research	000	2	9/16/2020	EXTENSION WITH OR WITHOUT FUNDS	$93,600
														Subtotal = $93,600

Grand Total All Awards = $364,010

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The mechanical role of the glycocalyx in cancer cell adhesion

Award Number: K00CA245789

ORGANIZATION: NATIONAL CANCER INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 09/16/2020

PERIOD OF PERFORMANCE END DATE: 11/30/2024

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