Table 1 Distinct influences of solid stress on tumor cell functions.

From: Biophysics in tumor growth and progression: from single mechano-sensitive molecules to mechanomedicine

Magnitude and direction of solid stress

Effects on tumor progression

Cell types

Mechanisms

Refs

4 mmHg

(Compressive)

Enhance cancer cell motility

Renal cancer cells (monolayer; in vitro)

Activate Akt/GSK-3β/β-catenin signaling pathway

[83]

4 mmHg

(Compressive)

Promote tumor cell migration

Pancreatic cancer cells (monolayer; in vitro)

Activate Akt/CREB1 pathway

[84]

5.8 mmHg

(Compressive)

Promote mammary carcinoma cell migration and adhesion

Breast cancer cells (monolayer; in vitro)

Enable the formation of leader cells and elevate cell-substrate adhesion

[85]

9 mmHg

(Compressive)

Enable oncogene activation and transform normal tissues into cancerous tissues

Healthy colon tissue (mouse)

Activate Ret and the downstream phosphorylation of β-catenin

[81]

15 mmHg

(Compressive)

Increase the motility of peripheral cells

Mouse colon carcinoma cells (multicellular spheroid)

NA

[82]

37.5-75 mmHg

(Compressive)

Inhibit multicellular tumor spheroid proliferation

Colon carcinoma cells; human breast cancer cells; mouse sarcoma cells (multicellular spheroid)

Induce the expression of the proliferation inhibitor p27Kip1

[87]

60 mmHg

(Compressive)

Suppress cell proliferation and induce apoptosis

Murine mammary carcinoma cells (multicellular spheroid)

Increase caspase-3 activity

[86]

45–120 mm Hg

(Compressive)

Inhibit the growth of multicellular tumor spheroids

Human colon adenocarcinoma cells; Murine mammary carcinoma; Rat rhabdosarcoma cells (multicellular spheroid)

NA

[88]